l^C  S'd'^ 


CA-^ 


ANATOMICAL  RESEARCHES 

ON  THE  SO-CALLED 

"PROSTATIC  HYPERTROPHY" 

AND 

ALLIED  PROCESSES 

IN    THE 

BLADDER  AND  KIDNEYS. 


BY 

6Ty\N15LAU5     C!ECHy\N0W5Kl 

Assistant  Professor  of  Pathological  Anatomy,  University 
of  Krakait,  Austria. 


y\UTliORlZED   TRAN6Ly\T10N 


EDITED  BY 

ROBERT  HOLMES  GREENE,  A.M.,  M.D. 

Genito- Urinary  Siirgeon  to  French  Hospital.     Sicrgeon  to     Work/iojtse 

and  Penitentiary  Hospitals,    N^cw    York   City.     Member  of  A?ner- 

ican  Association  of  Genito-Urinary  Surgeons,  etc. 


1903 
E.    R.  PELTON 

NEW    YORK 


EDITOR'S   PREFACE  TO  AMERICAN  EDITION. 

This  book  has  been  translated  as  the  result  of  an  agree- 
ment made  with  Prof.  Ciechanowski  some  months  ago.  It 
is  to  be  regetted  that  the  beautiful  plates  that  accompanied 
the  foreign  edition  have  been  destroyed  by  the  German  pub- 
lishers. The  views  of  the  Author  on  the  nature  of  the  pros- 
tatic hypertrophy  have  been  confirmed  by  the  editor  \vith  the 
valuable  aid  of  Dr.  Harlow  Brooks — see  "Fallacies  in  the 
Treatment  of  Urethral  Diseases,"  Journal  American  Medical 
Association,  1901,  and  "The  Nature  of  Prostatic  Hypertrophy, 
Journal  American  Medical  Association,  1902.  A  large  sale 
of  so  technical  a  work  as  this  is  not  expected,  but  it  is  be- 
lieved that  encouragement  should  be  given  to  the  production 
of  articles  on  pathological  anatomy.  The  Bibliography  at 
the  end  of  the  book  being  so  extensive  it  is  hoped  may  prove 
of  assistance  to  others  interested  in  these  or  topics  of  a 
similar  character  to  those  of  which  this  work  treats. 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/anatomicalresearOOciec 


INTRODUCTION 

Functional  disturbances  of  the  bladder  are  of  very 
frequent  occurrence  in  old  people.  In  most  cases  the 
trouble  lies  only  in  the  necessity  of  urinating  oftener 
than  is  usual;  but  in  many  cases  there  appear  much 
more  serious  symptoms,  either  there  remains  in  the 
bladder  a  smaller  or  larger  amount  of  residual  urine,  or 
an  absolute  retention  of  urine  takes  place,  or  there  is 
an  involuntary  overflow  of  urine  from  the  overfilled 
bladder.  This  functional  disturbance  is  usually  at- 
tributed to  an  enlargement  of  the  prostate  gland.  But 
it  is  a  well-known  fact  that  such  functional  disturbances 
take  place  also  in  cases  where  the  prostate  is  of  normal 
size;  yes,  even  when  it  is  below  normal  size. 

This  functional  disturbance,  which  I  shall  indicate  as 
bladder  insufficiency  of  the  aged,  appears  then  not  to  be 
in  absolute  connection  with  enlargement  of  the  pros- 
tate, which  is  commonly  called  "prostatic  hypertrophy." 
Cases  have  even  been  observed  where  the  bladder  has 
functioned  normally  in  spite  of  a  marked  enlargement 
of  the  prostate.  Furthermore,  it  is  proven  that  the 
prostate  is  by  no  means  enlarged  in  all  aged  men.  On 
the  contrary,  from  several  quarters  stress  is  laid  upon 
the  fact  that  disturbances  of  the  bladder  are  not  at  all 
a  general  condition,  but  occur  in  only  one-fifteenth  to 
one-twentieth  part  of  the  cases  where  there  is  prostatic 
hypertrophy.  The  different  varieties  of  bladder  insuf- 
ficiencv  in  the  aged  have  a  great  many  similar  clinical 


symptoms.  It  has,  however,  especially  in  recent  years, 
become  the  custom  to  group  all  these  varieties  together 
and  call  them  by  one  name.  People  were  even  con- 
vinced that  all  these  diseased  conditions  really  differed 
very  little  from  each  other,  and  that  they  only  represented 
different  stages  of  the  same  disease.  The  main  repre- 
sentatives of  this  view  are  Guyon  and  his  pupils,  who, 
for  the  last  twenty  years,  have  given  the  well-known 
name  "le  prostatisme"  to  this  disease.  This  name  is 
meant  to  represent  senile  bladder  disturbances  in  men 
and  in  women  as  well.  The  choice  of  the  same  proves, 
however,  that  the  author  is  convinced  that  such  bladder 
troubles  are  most  frequently  concurrent  with  enlarge- 
ment of  the  prostate  in  the  aged. 

The  characteristics  of  the  clinical  picture  are  only  to 
be  obtained  by  presenting  them  on  a  uniform  general 
anatomical  basis.  The  Guyon  school  tries  accordingly 
to  connect  all  urinary  symptoms  observed  in  a  lifetime 
with  similar  anatomical  changes  in  the  whole  genito- 
urinary apparatus.  The  characteristic  of  these  changes 
is  said  to  consist  of  sclerosis  of  all  the  tissues  and  parts 
of  this  apparatus.  They  state  the  sclerosis  attacks  mainly 
the  bladder  wall,  but  it  exists  at  the  same  time  in  the  kid- 
ney, testicle  and  prostatic  tissues,  by  which  the  prostate 
gland  in  most  of  the  cases  can  become  enlarged.  With  the 
exception  of  the  process  of  inflammation,  which  is  con- 
sidered an  accidental  complication,  all  changes  in  the 
different  divisions  of  the  genito-urinary  apparatus  are 
then,  according  to  their  school,  one  and  the  same 
thing.  They  are  all  called  forth  by  the  same  general 
cause  which  lies  outside  of  the  genito-urinary  apparatus, 
and  which  influences  the  whole  human  organism. 

According  to  the  older  statement  of  the  French  in- 
vestigators, this  general  and  common  cause  of  the 
anatomical  changes  in  the  bladder,  the  kidneys,  the 
testicles,  and,  in  certain  cases,  also   in   "prostatic   hyper- 


trophy,"  is  a  pure  influence  of  senile  changes.  Never- 
-theless,  the  following-  sentence  can  be  found  in  the 
famous  work  of  Guyon,  in  the  year  1885  (40  2d  ed., 
p.  119):  "C'est  sans  doute  I'age  des  malades,  qui  peut 
expliquer  les  inegales  conditions  de  la  resistance  de  la 
vessie  *  *  * "  (namely  by  the  comparison  of  the 
bladder  function  in  prostatic  hypertrophy  with  that  in 
the  cicatrical  chronic  gonorrhoeal  stricture  of  the 
urethra).  This  explanation  was,  however,  according  to 
all  appearances,  insufficient  even  for  Guyon  himself, 
because  he  then  took  refuge  in  the  overwhelming  in- 
fluence of  the  local  conditions,  i.  e.,  in  the  obstructions 
to  the  free  emptying  of  the  bladder  placed  by  the  pros- 
tatic hypertrophy  in  the  orificium  vesicale  urethra. 
"Jamais  ou  n'a  signale  chez  la  femme  de  la  retention 
senile,  jamais  ou  n'a  vu  sa  vessie  atteinte  d'inertie 
primitive.  A  quoi  peuvent  tenir  ces  immunites,  se  ce 
n'est  a  la  rectitude  et  a  la  permeabilite  de  I'urethre  qui 
restent  intactes  malgre  les  progres  de  I'age"  (1.  c, 
p.  120). 

At  this  time  there  came  an  important  change  in  the 
views  of  the  Guyon  school,  the  first  sign  of  which  ap- 
pears in  the  same  year  (1885)  in  the  publication  of  the 
thesis  of  Launois   [72]. 

Launois,  who  did  not  take  the  influence  of  old  age 
into  consideration,  was  the  first  one  who  expressly  in- 
dicated general  arterio  sclerosis  as  a  comimon,  general 
cause  of  the  anatomical  changes  in  the  whole  of  the 
genito-urinary  apparatus.  Like  the  well-known  my- 
ocardic  cicatrix,  caused  by  the  influence  of  the  at'hero- 
mata  of  the  coronary  arteries,  analogous  changes  in 
several  other  organs,  among  them  changes  also  in  all 
parts  of  the  genito-urinary  apparatus,  appear,  according 
to  Launois,  as  a  consequence  of  a  general  atheroma — 
i.  e.,  one  which  attacks  all  or  the  greater  part  of  the 
arterial  branches. 


In  tlie  kidney,  in  such  cases,  there  is  always  developed 
a  connective  tissue  hyperplasia  and  sclerosis,  which 
cannot  be  differentiated  from  the  usual  interstitial 
nephritis.  In  the  bladder  wall  there  appears  an  active 
connective  tissue  proliferation  at  the  expense  of  the 
bladder  muscles.  In  the  prostate  gland  the  connective 
tissue  has  an  active  part  in  the  growth  of  the  so-called 
fiibromyoadenomata,  which  really,  as  a  rule,  is  the  con- 
sequence of  the  arterial  atheroma  and  a  cause  of  the  so- 
called  "prostatic  hypertrophy." 

This  theory  of  Launois'  was  not  only  accepted  by  his 
teacher  in  its  full  extent,  but  was  even  drawn  with  still 
sharper  lines  and  stronger  colors.  Since  then  it  has 
been  maintained  and  enlarged  from  many  quarters,  and 
has  counted  followers  ever  increasing  from  day  to  day 
and  becoming  less  conservative,  although  very  soon 
weighty  objections  were  heaped  up,  first  in  Germany 
and  then  in   France. 

In  opposition  to  the  close  ranks  of  the  pupils  and  fol- 
lowers of  Guyon  stood  a  large  group  of  investigators, 
who  remained  faithful  to  an  older  view,  or  who  at  least 
gave  it  more  or  less  value.  It  was  in  general  always 
emphasized  by  this  group  that  the  cause  of  the  bladder 
disturbance  in  all  cases  lay  in  purely  local  changes  in  a 
part  of  the  urinary  or  genital  apparatus  respectively. 
To  such  local  causes  the  senile  bladder  insufficiency  has 
even  from  olden  time  been  attributed.  By  them  the 
changes  of  the  orificium  internum  and  of  the  pars 
prostatica  urethra  which  occur  in  the  great  majority  of 
cases  were  mainly  emphasized.  For  example,  Civiale 
emphasized  the  importance  of  th,e  condition  of  the  blad- 
der muscles  for  the  origin  of  interference  with  micturi- 
tion. It  is  Mercier's  great  merit  that  he  has  called  atten- 
tion to  the  previously  neglected  changes  in  the  so-called 
bladder  neck.  He  was  the  first  to  recognize  fully  their 
importance,   although  it  cannot   be  denied   that  he  has 


gone  a  little  too  far,  and  seems  to  have  forgotten  other 
conservative  factors. 

Civiale's  half-forgotten  view  has  in  its  main  lines  been 
renewed  by  Harrison  (58-60,  390-395).  Harrison  pre- 
sents it  in  a  way  which  is  much  too  fantastic  to  gain 
any  followers.  Harrison  asserts  that  the  main  object 
of  the  prostate  is  to  lift  the  bladder  fundus,  and  that 
the  prostate  must  suffer  a  working  hypertrophy  as  a 
consequence  of  primary  sclerosis  of  the  bladder  wall, 
which  brings  with  it  a  relaxation  and  deepening  of  the 
fundus  of  the  bladder. 

But  even  without  the  theory  of  Harrison  the  views 
of  Civiale  would  not  have  been  completely  forgotten, 
"mutatis  mutandis."  They  are  still  in  many  details 
preserved  in  the  Guyon  theory.  Mercier's  views  have 
generally  answered  for  this  in  the  literature,  even  if 
they  were  more  or  less  modified. 

The  enlargement  of  the  prostate  gland  then  is  by  many 
investigators  regarded  as  a  local,  primary  cause  which 
stands  at  the  head  of  all  other  changes,  and  on  which 
these  are  dependent.  But  they  by  no  means  agree  on 
the  questions  in  what  way  and  on  what  anatomical 
changes  this  enlargement,  which  usually  goes  by  the 
name  of  "prostatic  hypertrophy,"  depends.  Some  in- 
vestigators seek  the  cause  of  the  hypertrophy  outside 
the  prostate  gland  proper — namely,  in  the  influence  of 
the  activity  of  the  testes.  Others  think  that  the  cause 
lies  within  the  compass  ,of  the  tissues  of  the  prostate 
itself;  while  they  either  endeavor  to  draw  only  a  vaguely 
marked  parallel  between  the  uterus  and  the  prostate, 
or  point  to  a  previous  inflammatory  process  as  the  most 
important  etiological  factor.  The  theory  which  has  the 
m.ost  followers  is  that  all  anatomical  forms  of  enlarge- 
ment of  the  prostate  are  a  kind  of  new  growth;  they 
only  argue  over  whether  this  new  growth  comes  from 
the   epithelial   gland    elements,   or   from   the   interstitial 


muscle,  or  connective  tissue.  The  matter  is  still  more 
complicated  by  the  fact  that  the  great  majority  of  in- 
vestigators describe  several  special,  well-characterized 
forms  of  the  so-called  "hypertrophy." 

So  much  is  certain,  that  prostatic  hypertrophy  is 
by  no  means  the  only  cause  of  bladder  insufficiency  in 
old  people.  There  remains  a  large  number  of  cases 
which  are  not  accompanied  by  enlargement  of  the  pros- 
tate, the  so-called  cases  of  "Prostatisme  vesical." 

For  this  reason  it  seemed  to  me  proper  to  renew 
the  investigation  of  bladder  insufficiency  in  old  people. 
I  began  this  in  the  fall  of  1894,  and  continued  for  two 
successive  years,  and  was  assisted  in  it  by  my  much 
revered  chief  and  teacher.  Prof.  Browicz.  May  I  be 
permitted  here  to  express  my  gratitude  to  him,  not 
only  for  abundant  material,  but  also  for  the  strong  in- 
terest with  which  he  followed  my  work. 

Originally,  it  was  my  intention  merely  to  verify  the 
statements  made  by  the  Guyon  school;  but  the  work 
brought  forth  in  the  course  of  time  some  peculiarities, 
but  little  known,  which  seemed  to  me  adapted  to  throw 
some  light  on  the  pathogenesis  and  etiology  of  the 
whole  clinical  picture  of  "bladder  insufihciency  in  the 
aged,"  as  well  as  on  the  question  of  the  so-called  "pros- 
tatic hypertrophy." 

In  the  first  part  of  my  work  I  shall  consider  the 
alleged  g"eneral  causes  of  the  changes  in  the  genito- 
urinary system  in  the  course. of  the  so-called  "prosta- 
tismus,"  and  at  the  same  time  I  shall  give  the  re- 
sults of  my  investigation,  which  to  some  extent  will 
clear  up  the  question  of  senile  bladder  weakness. 
In  the  second  part,  I  shall  deal  with  the  pathological 
histology  and  the  etiologv  of  the  enlargement  of  the 
prostate,  to  which  the  name  "hypertrophy"  has  been  given. 


CHAPTER    I. 

ANATOMICAL  RESEARCHES  ON  THE  50=CALLED 

"PROSTATIC    HYPERTROPHY"  AND    ALLIED 

PROCESSES     IN     THE     BLADDER 

AND  KIDNEYS 

THE  SIGNIFICANCE   FCR  THE  ORGANISM    IN   GENERAL  OF  ATHEROMA. 

The  theon-  of  the  French  school  of  the  importance  of 
athromatons  changes  is  really  not  a  new  thought. 

It  originated  at  the  time  when  the  teaching  in  France, 
about  the  intiuence  of  general  atheromata  upon  the 
condition  of  all  the  organs,  found  its  development  and 
maturity.  And  since  that  time  the  atheroma  has  been 
recognized  as  a  very  important  and  far-reaching  factor; 
and  this  process  as  the  common  cause  of  a  great  group 
of  diseases,  which  were  looked  upon  before  as  due  to 
different  disturbances.  At  that  time  a  new  pathogenetic 
group  was  formed  to  which  the  name  of  "'Sclerose  gen- 
eralisee"  was  given. 

Guvon  and  his  pupils  had  at  hand,  therefore,  a  model 
to  follow,  but  they  had  only  what  was  at  that  time  a 
general  rule  to  use  for  the  special  cases. 

The  pathogenetic  significance  of  the  atheromatous 
processes  received  very  little  attention  before  the  forma- 
tion of  a  definite  understanding  of  the  general  scleroses 
of  the  internal  organs. 

Nearly  all  investigators  were  of  different  opinions  in 
regard  to  the  local  cause  and  development  of  the  athero- 
mata. Rokitansky  (286),  Schnopfhagen  (289),  Talma 
^293),  Ehrenreich  (264).  Mrchow  (296),  Langhans  ii-ji), 
Koster  (270-271).  Friedlander  (265),  Heubner-Traube 
(295),  Stroganow  (288),  Koster  (269),  Lancereux  {2'ji), 


Sternfeld  (292),  Thoma  (294). 

These  questions,  although  very  important,  have  no 
interest  for  us  at  present. 

But,  to  get  a  correct  understanding  in  order  to  ap- 
preciate the  pathogenetic  significance  of  the  atheromata, 
it  is  necessary  to  recollect  how  far  the  current  literature 
recognizes  the  active  part  played  by  the  small  arteries 
and  arterioles  in  atheromatous  processes,  and  how  this 
question  of  the  localization  of  atheromatous  changes  in 
the  different  arterial  ramifications  of  the  aorta  corre- 
sponds to  the  question  of  the  relative  frequency  of  the 
atheromata  in  the  different  parts. 

Some  of  the  investigators,  as,  for  instance,  von  Cornil 
and  Ranvier  (260-298),  Friedlander  (265),  and  others, 
separated  atheromata  of  the  arterial  branches  from  the 
changes  in  the  small  arteries  in  which  the  retrograde 
disturbances  of  nutrition  with  atheromatous  characteris- 
tics never  occur;  but  in  which,  on  the  other  hand,  the 
proliferative  and  hj'perplastic  processes  in  the  intima 
play  a  very  important  part. 

It  is  beyond  doubt  that  such  proliferation,  which  often 
leads  to  complete  obliteration  in  the  small  and  small- 
est arterioles,  often  stands  in  no  relation  to  the  athero- 
mata of  the  large  arterial  branches. 

It  is  a  well-known  fact  that  the  arterioles  which  are 
in  the  neighborhood  of  an  organ  suffering  from  chronic 
productive  inflammation,  share  after  a  time  in  the  same 
pathological  processes,  under  the  influence  of  the  same 
pathological  irritation  which  sets  up  the  inflammation  in 
the  organ  primarily  attacked,  and  will  be  obliterated  in 
time.  Similar  processes  are  observed,  as  is  well  known 
during  chronic  infectious  processes,  such  as  tuberculosis 
and  syphilis.  On  the  other  hand,  it  is  generally  known 
nowadays  that  the  pathological  picture  of  general  athe- 
roma with  the  proliferation  of  the  intima  of  the  small 
arteries  is  intimately  connected  with  that  of  atheroma 
of  the  aorta.  Truly  the  obliterating  endarteritis  of  the 
small  vessels  is  not  an  inevitable  result  of  the  atheroma, 
because  we  find  that  there  may  be  atheroma  of  the  larger 
vessels  without  the  smaller  ones  being  involved.  Be- 
sides this,-we  must  remember  that  in  old  people  there 
is,  as  a  rule,  a  moderate,  diffuse  thickening  of  the  ar- 
terial intima  which  must  be  regarded  as  physiological 

14 


and  within  certain  limits  a  normal  change  of  advanced 
life.  For  this  reason  it  would  be  very  desirable  to 
know  how  far  this  senile,  diffuse  thickening  of  the  in- 
tima  can  be  taken  for  a  normal  symptom,  and  at  what 
point  the  pathological  changes  begin  to  appear;  al- 
though a  mathematically  correct  border-line  cannot  be 
drawn. 

It  is  well  known,  however,  that  the  intima  in  every 
part  of  the  arterial  system  generally  appears  very  thin 
and  that  even  in  the  great  vessels  its  thickness  does 
not  exceed  .03  mm.  (Vierordt,  Anatomisch-physiolo- 
gische  Daten  u.  Tabellen  Jena,   1893). 

We  find  in  the  arteries  of  different  caliber  that  the 
relative  proportions  of  the  thickening  of  the  intima  to 
that  of  the  whole  of  the  vessel  wall,  as  well  as  of  the 
thickness  of  the  intima  to  the  diameter  of  the  lumen  are 
very  different;  just  as  the  thickness  of  the  wall  of  the 
arteries  differs  very  much  in  different  organs,  although 
their  lumen  is  the  same.  (Stahel.  Archiv  f.  Anatomic  u. 
Physiologic.  Anat.  Abt.  1886,  p.  45.)  For  this  reason 
alone,  no  one  up  to  the  present  day  has  tried  to  find 
the  absolute  measure  by  which  the  physiological  thick- 
ening of  the  senile  intima  may  be  differentiated  from 
the  moderate  pathological  changes. 

It  is,  however,  wholly  unnecessary  to  find  such  a 
measure,  inasmuch  as  we  examine  the  arterioles  of 
identically  the  same  organs,  and  for  comparative  group- 
ing we  only  select  arteries  of  nearly  the  same  caliber. 
A  relative  measure  is  more  than  sufficient  for  our  in- 
vestigation, since  we  shall  consider  only  the  advanced 
and  undisputable  intima  thickenings. 

In  the  small  arterioles  we  find  that  the  lumen  be- 
comes narrower  in  proportion  to  the  degree  of  the 
atheromatous  proliferative  obliteration,  and  that  the  wall 
becomes  continually  thicker  at  the  expense  of  the  lumen. 
This  fact,  which  is  considered  correct  by  all  other  iti- 
vestigators,  is  disputed  only  by  Thoma  (294),  (Virchow's 
Arch.  Bd.  71). 

Through  this  narrowing  of  the  small  arterioles  we 
can  best  explain  the  influence  of  the  atheroma  upon 
the  condition  of  the  affected  organs.  A  slow  diminu- 
tion of  the  nutritive  supply,  which  often  results  in  the 
complete  shutting  off  of  the  blood   supply,   must  nec- 

15 


essarily  produce  a  retrograde  disturbance  of  nutrition 
with  atrophy  O'f  the  component  parts  of  the  organ, 
which  are  replaced  by  connective  tissue  and  cicatrices 
(infarction).  We  see  every  day  on  the  dissecting  table 
advanced  examples  of  these  processes  in  the  form  of 
myocarditis  disseminata  fibrosa. 

The  results  of  the  arterial  atheroma  upon  the  organ- 
ism depend  entirely  on  whether  the  atheromatous 
changes  which  have  taken  place  in  the  large  arteries 
have  also  involved  the  smaller  ones.  If  in  addition  the 
small  arteries  are  involved  in  this  process,  the  physio- 
logical function  of  the  organ  will  suffer  damage,  which 
will  be  greater  the  more  numerous  the  branches  which 
are  affected. 

In  every  text-book  we  find  a  few  lines  at  least  about 
the  different  and  irregular  localization  of  the  atheroma. 

Rokitansky  in  his  table  of  frequency  (p.  310  and  227) 
places  the  common  iliac  fourth  and  the  hypogastric 
twelfth  in  frequency.  This  statement  has  often  been 
confirmed:  Curci  (259),  for  example.  He  found  in  93 
cases  of  atheroma  only  5  cases  of  the  hypogastric.  Von 
Bregmann  (258),  and  Mehnert  (281),  made  the  state- 
ment, founded  on  similar  experiences,  that  the  athero- 
mata  in  the  peripheral  arteries  decrease  in  frequency 
as  the  distance  from  the  heart  is  increased. 

It  will  be  seen  from  this  that  the  localization  of  the 
atheromata  is  very  irregular,  and  that  those  arteries  of 
the  small  pelvis  which  especially  interest  us  have  only 
a  small  tendency  toward  atheromatous  disease,  and 
lastly,  that  it  is  very  rare  to  find  a  general  arterial 
sclerosis  in  the  true  meaning  of  the  word. 

For  this  reason  alone  it  seems  impossible  to  accept 
the  statement  of  the  French  investigators  in  its  full 
extent,  without  criticism,  inasmuch  as  they  regard  the 
general  degeneration  of  the  connective  tissue  of  the 
internal  organs  (sclerose  generalisee)  as  due  frequently 
and  solely  to  the  changes  produced  by  arterial  atheroma. 

Even  to-day,  when  no  one  denies  the  pathogenetic 
importance  of  the  arterial  atheromata,  especially  of  the 
proliferative,  atheromatous  changes  in  the  small  ves- 
sels; the  number  of  pathological  processes  .which  are 
actually  caused  by  atheroma  is,  notwithstanding  this 
fact,  very  small.     Even  if  we  cross  the  borderline  of  the 

16 


fibrous  deg-eneration,  we  shall  find,  besides  the  euce- 
phalo-malachial  processes,  the  fibrous  myocarditis,  some 
forms  of  kidney-atrophy  and  the  so-called  senile  gan- 
grene, no  other  disease  which  stands  in  direct  and  un- 
disputable  dependence  upon  the  atheroma.  Also  the 
senile  atrophies,  so  often  encountered,  cannot  be  con- 
sidered without  much  ado  as  belonging  to  the  clinical 
picture  of  the  so-called  "sclerose-generalisee."  These 
simple  atrophies  could  as  well  be  a  process  independent 
of  an  atheroma;  at  the  most,  perhaps,  one  coordinated 
to  it. 

There  are,  therefore,  considerations  "a.  priori" 
against  the  causative  connection  maintained  by  the 
Guyon  school,  of  the  hypertrophy  of  the  prostate  gland 
and  the  accompanying  symptoms  of  the  arterial  athe- 
roma. 

In  order  to  prove  the  lack  of  foundation  for  this  the- 
ory, which  at  any  rate  is  intelligent  and  clever,  there  is 
call  for  direct  proof  that  hypertrophy  of  the  prostate 
gland  and  bladder  insufficiency  are  not  constantly  ac- 
companied by  atheroma  of  the  vessels  supplying  the 
genito-urinary  apparatus.  At  the  outset  it  is  not  to 
be  disregarded  that  atheroma  of  the  pelvic  and  renal 
arteries  occurs  with  a  certain  regularity,  in  spite  of  the 
fact  that  the  vessels  in  other  parts  of  the  body  may  be 
normal. 

The  irregularity  and  unevenness  in  the  localization 
of  the  atheromatous  processes  in  different  branches  of 
the  arterial  system  makes  this  seem,  at  least,  iiot  im- 
possible. 


17 


CHAPTER    11. 

THE     inPORTANCE     OF     ARTERIAL     ATHEROflA 
IN     THE     GENITOURINARY     ORGANS 

The  number  of  investig-ations  up  to  the  present  day 
which  treat  directly  of  the  frequency  and  locahzation  of 
the  atheromatous  process  in  the  dominion  oif  the  genito- 
urinary apparatus  is  very  small  indeed.  In  the  thesis  of 
Launois  {y2)  it  is  tO'  be  regretted  that  nothing  definite 
concerning  the  subject  is  to  be  found.  Also  in  the  works 
of  Bohdanowicz  (7),  and  Motz  (89B),  there  are  very  few 
details.  Motz  says  that  he  found  among  30  cases  of 
hypertrophy  of  the  prostate  gland  9  cases  oi  sclerosis  of 
the  small  arteries  within  the  gland  itself.  Really  correct 
investigation  is  only  to  be  found  in  Casipar's  work  (16). 
Among  24  cases  of  hypertrophy  of  the  prostate  gland 
with  atheroma  of  the  aorta  he  found  atheroma  in  the 
renal  arteries  and  in  the  main  branches  of  bladder  vessels 
in  8  cases ;  in  the  small  arteries  within  the  bladder-wall 
in  9  cases ;  but  changes  in  the  small  prostatic  arteries  in 
only  4  cases.  A  general  atheromatous  process  of  all  the 
arteries  of  the  genito-urinary  system  he  found  only  in  2 
cases. 

The  results  of  my  own  investigation  are  shown  in  table 
No.  I. 

This  group  relates  to  42  male  and  5  female  cadavers  of 
old  people  with  a  condition  of  more  or  less  high-grade 
arterial  atheroma. 

In  one-half  of  the  male  bodies  examined,  all  of  Which 
except  4  were  over  50,  and  the  majority  between  60  and 
70  years  old,  a  hypertrophy  of  the  prostrate  gland  was 
found  going  beyond  the  normal  dimensions. 

Among  these  21  cases  with  hypertrophy  of  the  prostate 

18 


gland  I  found  atheromatous,  atheromatously-prolifera- 
tive  changes,  respectively,  in  21  cases  in  the  aorta,  in  18 
cases  in  the  common  ihac  and  hypogastric,  in  7  in  the 

TABLE   I. 

The  co-incidence  of  the  Arterial  Atheroma,  Kidney  Degenerations  and  Enlarge- 
ment of  the  Prostate. 


V 
X 

1 

"5 

5;  a: 

^:\ 

1 

th 
Org 

kin 

Condition 

0/ 
Kidneys. 
Formed 

1 

NOTE 

1 

"6- 
1 

3 
4 

I 

7 
8 

•3 

il 
■7 

■s 
58 

59 

69 
76 
68 
67 
77 
72 
75 
80 
69 
78 
63 

60 
67 
74 
78 
70 
65 
75 
77 

1 

[ 

; 

Atrophia  senilis 
Cirrhos.  e  arterioscl 
Cicalr.  post  infarct. 

Atrophia  senilis 

A.  sen.  et  Nephr.  apost. 
.Atrophia  senilis 

Cicatr.  post  intarct. 

Pyelitis  calculosa 
Nephritis  chronica 
Degeneratio  cystica 

31.2 
25.0 

13-5 

■5-3 

15.6 
26,6 
26.0 

39 -o 
30.8 
36.2 
28.7 
30.0 
27.3 

40.4 

Atheroma  of  art.  0.'  extremities  and  brain 
"            "  all  art.  except  pulmonary 
"            "  covonai7  art. 

"  the  whole  art.  system 
"  "     covonary  arteries 

"            "  ■'■           "  and  cerebral  art. 

"            "  "  cerebral  an. 

"             ■'  "  covonary  and  extrem.  an. 

^ 

2, 

■  8  1 

8    7 

7 

8 

2 

7 

21 

^3 

25 
26 
27 
28 
-9 
30 
3' 
32 
33 
34 

11 
37 
38 
39 
4<: 

65 
75 
45 
57 
67 
59 

40 
53 
75 
40 
57 
70 
62 
68 
72 
70 

11 
60 

74 

\ 

'' 

■ 

■ 

' 

■ 

Cirrhos.  e  arterioscl. 

Atrophia  senilis 

Nephritis  chronica 

Cirrhos.  e  arterioscl. 
Atrophia  senilis 
Nephritis  acuta 

Nephritis  acuta 
Amyloidosis 
Hyperaemia  passiva 

Nephritis  chronica 
Cirrhos.  e  arterioscl. 

■7 

'7 
'3 
13 
16 
18 

'9 

'9 
15 

la 

'9 

5 
5 

3 
4 
4 

6 

4 
6 

5 
8 

8 

Atheroma  of  arteries  of  extremities 
"          "  covonary  arteries 

Atheroma  generalisatum 

"        covonary  and  extrem.  an. 

"        Covonary  art. 
"        generalisatum 

-a 

■■ 

0    8 

8 

9 

8 

3 

21 

iS 

43 

29 

8.5 

15 

■  7 

lo 

10 

Cirrhos.  e  arterioscl.      4 
Nephritis  chronica          ■ 
Atrophia  senilis  7        (8) 
Other  degen.                  10 
No            "                      18 

21 

21 

Atheroma  generalisatum        4 

cerebral  art.              i  U)  , 
covonary  art.            9  (13) 
Art.  otherwise  normal             22 

5 

4 
4 

4 

go 
70 
70 
74 
8r 

; 

I     j 

1 

1 
I 

Atropliia  senilis 
Cirrhosis  e  arterioscleros 

(^ 

4 

5 

5    3 

■• 

4 

Cirrh.  e  arterioscl.  i,  A. 4 

arteries  of  the  bladder  and  prostrate  gland  (before  they 
entered   the   substance   of  this   gland),  in   8  in   arteries 


19 


within  the  bladder-wall,  in  2  in  the  arterioles  of  the  pros- 
tate gland,  and  in  7  in  the  renal  arteries.  In  the  other 
half  O'f  the  cases,  those  without  hypertrophy  of  the 
prostrate  gland,  I  found  arterio-sclerosis  19  times  in  the 
aorta,  11  times  in  the  common  iliac  and  hypogastric,  8 
times  in  the  main  branches  of  the  bladder  and  the  pros- 
tate gland,  9  times  in  the  arterioles  of  the  bladder-wall,  8 
times  in  the  arteries  within  the  prostate  gland,  and  only 
3  times  in  the  renal  arteries. 

In  this  place  stress  must  be  laid  upon  the  fact  that  I 
reckoned  only  those  vessels  affected  by  atheromatous  de- 
generation, in  which  there  existed  either  an  indisputable 
endarteritis  nodosa  or  a  thickening  of  the  intima,  quite 
regular  and  diffuse,  but  overstepping  the  normal  limits  of 
the  pathological,  as  was  proven  'by  miscroscopic  meas- 
urements. 

In  all  the  five  female  cadavers  I  found  arterio-sclerosis 
in  the  common  iliac  and  hypogastric ;  in  four  I  found  it  in 
the  renal  vessels,  in  the  small  vessels  of  the  bladder  and 
in  the  aorta ;  in  three  of  the  cases  the  main  branches  of 
the  vessels  of  the  bladder  were  attacked  by  the  arterio- 
sclerosis. 

To  sum  up,  the  investigation  of  the  forty-two  cases 
showed  arterio-sclerosis  in : 

Aorta 40  times 

Common  iliac ; 29 

Hypogastric 29      " 

Main  branches  of  vesicle 15 

Large  branches  of  prostate 15      " 

Vesicular  branches  within  bladder  wall 17      " 

Prostatic  vessels  within  the  gland 10      " 

Renal  arteries 10      " 

Besides  these  I  found  atheroma  in  : 

Coronary  arteries 13      " 

Basilar  arteries 4      " 

Arteries  of  extremities 4      " 

Finally  there  was  a  general  atheromatous  process  in 
four  cases,  in  two  of  which  (case  2  and  6)  there  was  at 
the  same  time  an  hypertrophy  of  the  prostate  gland. 

The  concurrent  appearance  of  the  arterio-scherosis  in 
the  renal,  vesicular  and  prostatic  arteries  was  found  seven 
times;  among  these,  four  times  together,  with  an  hyper- 
trophy of  the  prostate  gland.     (Case  2,  6,  15,  17.) 


All  vessels,  with  the  exception  of  the  arterioles,  of  the 
genito-urinary  system,  showed  a  general  arterio-sclerotic 
change  in  three  cases  (case  20,  28,  40)  ;  in  none  of  which 
a  hypertrophy  of  the  prostate  glared  could  be  proven. 

Among  the  fifteen  cases  in  which  there  were  athero- 
matous changes  in  the  larger  vesicular  and  prostatic  ar- 
teries, the  prostate  gland  was  found  of  normal  size  in 
five  cases  (case  24,  28,  38,  39,  40)  ;  small,  atrophic,  and 
fromi  twelve  to  twelve  and  a  half  grams  in  weight  and  in 
three  cases  (case  20,  31,  33;  and  large  in  seven  cases. 
In  the  remaining  fourteen  cases  of  hypertrophy  of  the 
prostate  gland  all  signs  of  arterio-sclerosis  of  the  pros- 
tatic vessels  were  missing. 

This  table,  which  was  formed  by  myself,  does  not  ex- 
actly coincide  with  the  results  of  Curci,  Mehnert  and 
Bregman ;  but  the  small  difference  existing  cannot  over- 
throw the  rule  formulated  by  these  investigations,  that 
the  frequency  of  the  atheroma  in  the  peripheral  vessels 
decreases  the  further  they  are  from  the  heart.  Exception 
to  this  rule  is  found  in  my  cases  in  the  renal  arteries  only. 

Even  if  this  general  rule,  confirmed  once  more  by  my 
investigation,  seems  to  weaken  the  Guyon  theory,  yet  we 
cannot  entirely  forsake  it.  von  Launois  (72  p.  102)  lays 
stress  upon  the  fact  that  the  changes  in  the  kidneys,  blad- 
der and  prostate  gland  are  only  synchronous,  co-ordinated 
and  anatomical  consequences  of  one  and  the  same  cause, 
i.  e.,  an  endoperiarteritis  of  the  small  vessels,  and  that  be- 
tween the  changes  in  the  vessels  and  the  "sclerose"  of 
these  three  organs  there  is  a  strong  parallelism ;  in  other 
words,  that  the  extent  and  intensity  of  these  changes  of 
the  organs  get  to  be  more  marked  the  more  the  vessels 
are  attacked  by  this  atheromatous  process.  On  the  basis 
of  the  cited  results,  obtained  by  myself,  it  can  at  most 
be  stated  that  the  changes  in  the  vessels  of  the  entire 
genito-urinary  system  are  neither  constant  nor  synchron- 
ous with  each  other  in  cases  of  hypertrophy  of  the  pros- 
tate gland. 

The  question  whether  the  changes  in  the  tissues  of  the 
genito-urinary  system  are  really  analogous,  and  whether 
there  exists  a  strong  parallelism  between  the  extent  and 
intensity  of  atheromatous  changes  in  the  vessels  and  the 
fibrous  degeneration  of  the  kidney,  bladder  and  prostate 
must  still  remain  undecided. 


The  decision  of  these  questions  is  possible  only  through 
a  careful  investig'ation  of  the  condition  of  the  vessels  and 
the  condition  of  the  organs,  i,  e.,  the  kidneys,  bladder  and 
prostate. 


CHAPTER  III. 

RELATION  OF  ARTERIAL  ATHEROMA  TO  THE 
POST  ATE  GLAND 

It  is  is  not  difficult  to  prove  that  no  causative  connec- 
tion exists  between  the  enlargement  of  the  prostate  gland, 
which  is  cornmonly  known  as  hypertrophy  of  the  prostate 
gland,  and  the  arterio-sclerosis. 

It  seems  a  "priori"  hardly  possible  to  find  such  causa- 
tive connection,  because,  as  was  first  pointed  out  by  Cas- 
par (i6),  the  disease  processes,  in  which,  on  account  of 
arterial  sclerosis,  an  enlargement  of  the  involved  organ 
might  take  place,  are  altogether  not  known  and  not  possi- 
ble. Moreover,  even  by  the  Guyon  school  itself  protest 
was  made  against  the  conception.  See  Bohdanowicz  (7), 
Motz  (89B  p.  43),  It  is  really  hard  to  understand  why 
Launois,  who  followed  a  road  made  by  his  coumtr^-men, 
seemed  to  forget  a  very  important  part  of  the  French 
theory.  Martin,  Duplaix,  Martha,  Lancereux  and  others 
mention,  in  their  teachings  of  the  so-called  "sclero'se 
generalisee,"  only  cirrhosis,  atrophy,  and  such  atrophic 
conditions  of  the  organs  as  are  accompanied  by  shrinkage 
and  are  entirely  due  to  a  general  arterial  sclerosis. 

The  condition  of  the  larger  prostatic  arteries,  which  I 
mentioned  before,  and  which  we  shall  lay  aside  for  the 
present,  will  only  point  out  that,  among  my  forty-two 
cases  of  really  advanced  arterial  sclerosis,  in  ten  cases 
only  was  there  found  an  atheromatous,  proliferative 
change  of  the  same  vessels  within  the  prostate  gland. 
Among  these  ten  cases  of  atheroma  of  the  smaller  of  the 
prostatic  vessels  the  prostate  gland  was  only  once  atro- 
phic (case  20),  and  twice  hypertrophied  (case  2.19); 
the  weight  was  25  and  27.3  grams  respectively.     In  all 

23 


the  other  cases  of  even  advanced  prostatic  hypertrophy 
the  intra-prostatic  vessels  were  found  normal.  In  the  re- 
maining- seven  cases  of  atheroma  the  prostate  gland  was 
found  unchanged  (case  23,  28,  29,  37,  38,  39,  40).  Among 
the  cases  of  Bohdanowicz  we  find  one  (No.  II)  which 
treats  of  an  old  man  of  seventy-five  years  with  intense 
hypertrophy  of  the  prostate  gland  zvithout  any  sign  of  ar- 
terio-sclerosis. 

An  analogous  observation  was  made  by  myself  (case 
8).  A  man,  80  years  old,  had  atheroma  in  the  ascending 
aorta,  arch  of  the  aorta  and  coronary  arteries  ;  the  pros- 
tate g'land  was  visibly  enlarged,  weighing  34  grams,  and 
showed  a  pathological  change  in  structure. 

These  two  observations  alone  are  sufficient  to  conti*a- 
dict  the  statement  of  Guyon,  that  persons  who  escape  the 
atheromatous  process  will  have  no  enlargement  of  the 
prostate  gland  (85,  p.  1.09). 

The  conclusions  w'hich  may  easily  be  drawn  from  the 
facts  already  cited  appear  to  be  better  justified  if  one  con- 
siders that  in  these  cases,  in  which  the  atheromatous 
changes  in  the  intra-prostatic  arteries  were  met,  the 
changes  were  very  irregular  among  the  arterial  branches 
and  differently  supplied  parts. 

The  one,  and  only,  rule  (and  this  is  open  to  very  many 
exceptions)  is  the  relatively  frequent  localization  of  the 
atheromatous  processes  in  the  larger  arterial  branches, 
which  terminate  in  the  periphery  of  the  prostate  gland. 

In  contradistinction  arterio-sclerotic  changes  were 
less  frequently  observed  among  the  ramifications  of  the 
•arterial  system  within  the  parenchyma  of  the  prostate 
gland. 

It  deserves  to  be  mentioned,  in  addition,  that  I  counted 
among  the  pathological  cases  of  the  prostate  gland,  not 
'Only  those  cases  in  which  the  arterio-sclerotic  changes 
were  very  pronounced,  but  also  those  in  which  only  a 
■few  or   even    a    single    arteriole    showed    atheromatous 

Owing  to  the  fact  that  a  border-line  cannot  be  sharply 
drawn  between  the  physiological-senile,  and  the  patho- 
logical, thickening  of  the  intima  ;  I  counted  also  as  patho- 
logical all  the  prostatic  arterioles  in  which  the  intima 
thickening  and  narrowing  of  the  lumen  was  small,  but 
still  reached  beyond  the  highest  limit,  which  was  found 
hy    measurinsf    the    thickness    of    the    int'.ma    and    the 


24 


diameter  of  the  lumen  of  vessels  of  young  people,  who 
surely  were  not  attacked  by  atheroma. 

In  considering  atheromatous  changes  I  intentionally 
left  the  condition  of  the  adventitia  unregarded.  It  is  easy 
lor  one  to  satisfy  oneself  as  to  the  fact  that  the  adventitia 
of  the  intra-prosratic  vessels,  especially  of  the  vessels  of 
the  periphery,  is  normally  conspicuously  thick.  We  are 
therefore  not  justified  in  assuming  that  the  thickening  of 
the  adventitia  is  a  sign  of  arterial  sclerosis.  Besides  this 
it  is  well  known  that  the  thickness  of  the  adventitia  is 
very  irregular  in  the  normal  state ;  on  the  one  hand,  with 
regard  to  the  region  of  the  body  and  the  arterial  branches 
of  one  and  the  same  individual,  and  on  the  other  hand  as 
regards  the  same  arterial  branches  in  different  individ- 
uals. For  this  reason  I  came  to  the  conclusion  that  it  is 
not  sufdcient  for  the  diagnosis  of  atheromatous  changes 
to  take  the  thickness  of  the  adventitia  into  account.  One 
must  base  one's  diagnosis  upon  the  proof  of  calcification 
or  other  retrograde  metamorphoses,  or  on  the  round-cell 
infiltration  within  the  adventitia.  Launois,  on  the  con- 
trar}^,  took  the  thickening  of  the  adventitia  as  a  charac- 
teristic matter  of  principle  in  his  account  of  the  arterio- 
sclerosis O'f  the  vessels  of  the  genito-urinary  apparatus 
even  in  those  vessels  in  which  there  was  no  intima  thick- 
ening. He  says  that  every  artery  which  terminates  in 
the  periphery  of  a  hypertrophied  prostate  gland,  "toutes 
sans  exception,"  is  surrounded  by  a  ring  of  connective 
tissue.  This  assertion  is  very  remarkable.  I  am  inclined 
to  assume  that  for  Launois  a  normal  condition  was  soane- 
thing  pathological,  and  that  he  was  led  through  this  mis- 
take oil  a  wrong  track,  at  least  with  regard  to  the  pros- 
tate gland. 


25 


CHAPTER    IV. 

RELATION    OF    THE      ARTERIAL    SCLEROSIS    TO 
THE  KIDNEYS 

Gull  and  Sutton  (202),  in  the  year  1872,  first  called  at- 
tention to  the  changes  in  the  kidneys  produced  by  the 
disease  processes  in  the  arteries  ;  but  they  did  not  define 
the  relation  of  the  well-known  "arterio-capillary  fibrosis" 
to  the  arteriol  sclerosis.  The  teaching  of  Gull  and  Sut- 
ton, which  for  10  years  was  the  starting-point  for  numer- 
ous debates,  found  only  a  few  followers  in  its  original 
form.  Notwithstanding  this  it  had  a  great  influence  on 
the  completion  and  development  of  the  teaching  of  the 
so-called  "sclerose  generalisee"  and  also  on  the  defini- 
tion of  the  idea  O'f  arterio-sclerotic  shrinkage  of  the  kid- 
ney. The  most  important  arguments  against  the  Gull- 
Sutton  teaching  were  made  by  Grainger-Stewart 
(206-209),  and  Hood  (218),  then  by  Rindfleisch  (311), 
Cohnheim  (299)  and  Bartels  (181).  The  latter  believed 
that  Gull  and  Sutton  had  "evidently  confounded  the 
senile  changes  of  the  kidneys  wath  the  real  and  genuine 
shrinkage  of  the  kidney,  from  affection  for  their  newly 
created  Morbus-Brighti-Idea"  (1  c.  p.  371.)  If  I  be  not 
mistaken,  Henouille  (217),  a  pupil  of  Lancereux,  em- 
phasized What  had  already  appeared  in  some  works,  but 
was  established  by  Henouille,  is  a  clear  etiological  under- 
standing, and  has  nothing  to  do  with  an  anatomically 
limited  form  of  disease.  The  majority  of  investigators, 
with  the  exception  of  Ewald  (200)  and  Thoma  (252),  who 
in  the  following  years  have  concerned  themselves  with 
this  subject,  have,  in  this  sense,  accepted  the  arterio- 
sclerotic shrunken  kidney  as  a  purely  etiological  idea. 
In  this  connection  the  works  of  Erault  (185),  Cornil  (192, 

26 


I93)>  Mahomed  (234),  Senator  (245),  Petrone  (240), 
Lemcke  (227),  Amburger  (178),  Meigs  (237,  238),  a.  0., 
should  be  read.  In  the  anatOimical  picture  entire  tlie 
simple  senile  atrophy  of  the  kidney  is  still  added,  and 
this  means  that  the  conviction  is  expressed,  especially  in 
the  old  French  works,  that  all  atrophic  conditions  of  the 
kidney,  as  found  in  old  people,  are  identical  with  the  in- 
flamed shrunken  kidney,  and  without  exception  caused 
by  arterio-sclerosis.  As  followers  of  this  view  it  is  suf- 
ficient to  mention  Lemoine  (231),  Dumange  (196),  De- 
bove  and  Letulle  (195),  but  especially  Sadler  (248). 

Launois  accepted  Sadler's  views  in  their  full  extent/ 
although  he  was  familiar  with  the  divergent  and  well- 
founded  ideas  of  Ballet  (179),  as  well  as  with  the  ideas 
of  Cornil  and  Brault  (192).  The  border-line  between 
the  senile  kidney  atrophy  and  the  arterio-sclerotic 
shrunken  kidney  was  likewise  missing  in  the  later  works 
of  Lancereux  (233)  and  Grancher  (213),  and  in  the 
monographs  of  Bull  (180)  and  Lowenfeld. 

The  development  O'f  the  anatomical  conception  of  the 
arterio-sclerotic  shrunken  kidney  and  its  exact  separa- 
tion from  the  related  forms,  i.  e.,  the  simple  senile  atro- 
phy and  the  inflamed  and  genuine  shrunken  kidney, 
is  especially  due  to  the  German  investigators,  Weigert 
(256)  and  Leyden  (229),  but  particularly  to  Ziegler  (257). 
To  the  excellent  anatomical  characteristics  of  these  three 
conditions,  as  tabulated  by  the  latter,  nothing  can  even 
now  be  added.  It  was  confirmed  by  Rosenstein  (244). 
Biermer  (186),  Dunin  (194),  Lemcke  (227),  o.  a.;  and 
will  finallv  be  incorporated  in  all  newer  manuals  and 
textbooks' (at  least,  in  the  German  books).  In  the  man- 
ual of  Orth  (310),  there  is  toesides  a  very  exact — per- 
haps the  most  exact — description  of  the  differential  di- 
agnostical  characteristics  of  these  three  forms. 

The  number  of  the  treatises  which  in  the  widest  sense  of 
the  word  treat  of  the  atrophic  charges  of  the  kidneys  is 
very  large  indeed.  , 

The  relation  between  the  arterial  sclerosis  and  the 
atrophy  O'f  the  kidney  with  its  accompanying  changes  was 
for  a  long  time  a  "terra  incognita." 

The  majority  of  the  chronic  processes  O'f  these  organs 
were  treated  as  belonging  to  a  common  group.  They 
were  called  bv  different  names  with  the  same  luraning, 


27 


as  :  Cirrhosis  of  the  kidney,  sclerosis  of  the  kidney,  granu- 
lar atrophy  of  the  kidney,  chroiiic  inflammation  of  the 
kidney,  interstitial  nephritis,  shrunken  kidney,  etc. 

Only  through  the  efiforts  of  later  years  has  it  been  pos- 
sible to  classify  the  real  renal  atrophies  "sensu  stricto" 
and  set  them  apart  from  those  occurrences  which  accom- 
pany the  shrinking  of  the  organ,  but  are  never  due  to 
simple  disturbance  in  nutrition.  Among  the  simple  atro- 
phies there  is  a  well-characterized  and  well-limited  form, 
the  so-called  "arterio-schlerotische  Schrumpfmere  (atro- 
phia e  origine  vasculosa,  ren  arterioskleroticus).  It 
is  directly  due  to  the  atheromatous  process  in  the  renal 
arteries  and  their  branches. 

A  strict  dififerential  diagnosis  is,  in  spite  of  this,  some- 
times ver}^  difficult,  and  now  and  then  even  impossible. 
In  such  cases,  which  are,  by  the  way,  very  rare,  noth- 
ing remains  but  to  diagnosticate  them  as  a  transitional 
form.  In  the  great  majority  of  cases  we  meet  with 
clear,  and,  as  a  rule,  easily  diagnosed  forms. 

Simple  senile  atrophies  of  the  kidney  belong  to  the  dailv 
finds  of  the  dissecting  room.  Both  kidneys  are  in  svich 
cases  uniformly  small.  Their  weight  is  generally  20-30 
grams  less  than  ihat  of  the  normal  kidneys  (left  80-90, 
instead  of  100-120;  right  70-80,  instead  of  90-ioog.). 
The  form  of  the   kidneys  remains  unchanged. 

The  covering  of  fat  increases  often  in  thickness,  es- 
pecially in  the  region  of  the  hilus.  The  capsule  proper 
is  easily  torn  ofT,  and  is  thin.  The  surface  of  the  kid- 
ney is,  in  the  simple  senile  atrophy,  either  smooth,  or, 
what  is  more  frequent,  uniformly  finely  granular  and 
of  a  uniform,  reddish-brown  color.  The  cortical  sub- 
stance appears  in  the  cut  section  uniformly  smaller, 
but  its  characteristic  radiating  lines,  as  well  as  the 
boundary  line  between  it  and  the  medulla,  are  pre- 
served. Sometimes  small  cysts  are  seen,  which  are  lo- 
cated either  on  the  surface,  or  in  the  parenchyma;  and 
contain  a  clear  serum  or  a  gelatinous,  transparent,  yel- 
lowish mass.  The  arterial  branches  in  the  parenchyma, 
which  can  be  seen  with  the  naked  eye,  are  unchanged. 
The  main  trunk  of  the  renal  artery  may  either  be 
normal,  or  it  may  be  the  seat  of  atheromatous  changes 
of  varying  intensity  and  extent. 

In  my  investigation,  I  have  recorded  these  cases  just 

28 


described  as  simple  senile  atrophy,  provided  that  no 
symptoims  of  albuminuria  were  present  during  lifetime. 
The  atrophic  condition  of  the  uriniferous  tubules  and  the 
malphigian  bodies  is  very  characteristic  under  the  mi- 
croscope, in  the  cases  of  simple  senile  atrophy.  The 
malphigian  bodies  become  smaller  and  their  characteris- 
tic outline  becomes  gradually  lost;  their  capillaries  lose 
the  endothelial  cells,  are  now  and  then  attacked  by  hya- 
line degeneration,  and  finally  collapse  and  lose  their 
lumen. 

The  final  outcome  of  this  process  is  a  hyaline  de- 
generation and  a  complete  wasting  away  of  the 
shrunken  glomerulus  to  a  homogeneous  ball.  The 
decrease  in  size  of  the  senile  kidney  is  mainly  caused  by 
the  atrophic  condition  of  the  uriniferous  tubules.  The 
lumen  of  these  becomes  gradually  narrower:  the  epi- 
thelial cells  lose  their  characteristic,  differentiating 
marks;  they  become  flatter,  smaller,  cuboidal;  they  lose 
their  sharp  outline,  and  their  nuclei  are  smaller  and 
stain  more  strongly. 

The  interstitial  connective  tissue  is  as  a  rule  un- 
changed: Sometimes  we  find  the  capsule  of  the  glome- 
rulus slightly  thickened,  and,  still  rarer,  we  now  and 
then  observe  a  few  rotmd-cell  infiltrations.  It  is  beyond 
doubt  that  these  characteristic  changes  of  a  senile  kidney 
atroph}^  are  due  to  a  disturbance  in  nutrition — a  de- 
creased blood  supply.  But  one  should,  as  Ziegler  cor- 
rectly states,  in  every  individual  case,  consider  as  to 
whether  the  general  senile  involution  of  the  tissue  and 
the  decrease  in  the  entire  blood  supply  is  due  to 
decrease  in  the  activity  of  the  heart,  a  diseased  main 
branch  of  the  aorta,  or  to  the  condition  of  the  cells  of  the 
parenchyma  of  the  kidneys.  The  main  importance  may  lie 
in  the  changes  in  the  heart,  or  in  the  main  arterial 
branches,  or  in  a  general  marasmus  (1.  c.  p.  6oi).  Corre- 
sponding to  the  main  factor  that  attacks  the  whole  organ- 
ism both  Kidneys  are,  almost  without  exception,  at- 
tacked by  simple  senile  atrophy  when  it  exists,  and  in  each 
kidney  the  atrophic  changes  are  diffuse,  i.  e.,  evenly  dis- 
tributed in  all  its  component  parts.  The  arterio-sclerotic 
shrunken  kidney,  which  in  its  pure  form  is  to  be  classi- 
fied among  the  senile  kidneys,  as  both  are  due  to  sim- 
ple  retrograde   disturt)ances   of   nutrition,   differs   only 

29 


from  tlie  senile  kidney  in  that  it  is  caused  by  certain 
local  inlluences.  According  to  whether  the  left  or  the 
rig'ht  renal  artery  is  attacked  by  an  atheromatous  proc- 
ess of  greater  intensity  and  extent,  the  left  or  the 
right  kidney  will  suffer  the  greater  changes.  Thus  we 
will  sometimes  find  an  arterio-sclerotic  shrunken  kid- 
ney on  one  side;  while  the  kidney  on  the  other  side 
sho'ws  little  or  no  changes,  or  only  a  simple  senile 
atrophy.  Besides  this,  corresponding  to  the  irregular 
localization  and  intensity  of  the  arterial  sclerosis  in  the 
individual  branches  of  one  of  the  renal  arteries,  wie  find 
that  the  localization  and  the  degree  of  the  arterio- 
sclerotic parenchymatous  changes  are  uneven  in  the 
different  parts  of  the  same  kidney.  Therefore,  the  an- 
atomical picture  of  an  arterio-sclerotic  shrunken  kidney 
is  more  varied  than  that  of  a  simple  senile  atrophy  of 
the  kidney.  In  those  cases  in  which  the  atheromatous 
process  attacks  evenly  the  smallest  branches  of  the 
renal  artery,  the  kidney  will  become  evenly  smaller. 

Tlie  somewhat  thickened  capsule  generally  found  in 
such  cases  is  easily  removed  from  the  coarse,  granular 
surface.  Those  projecting  granules  are  generally  of  a 
palvT  color  than  the  grooves  between  them.  The  pa- 
renchyma is  of  a  dark-red  color,  and  its  characteristic 
contour  is  very  indistinct.  The  section  of  the  arteries 
in  tlic  parenchyma  which  are  visible  to  the  naked  eye 
is  rigid  and  does  not  collapse.  The  arterial  walls  are 
very  unevenly  thickened,  and  the  lumen  is  also  greatly 
increased,  especially  in  the  larger  arteries,  less  in  the 
smaller  ones.  Sometimes  we  find  small  cysts,  the  size 
of  a  pea,  within  the  connective  tissue. 

If  the  artificial  sclerosis  attacks  individual  branches 
only,  or  if  the  arterio-sclerotic  process  is  of  different 
intensity,  then  the  kidneys  'become  unevenly  smaller. 
On  the  surface  we  observe  broad,  flat,  intersecting 
grooves  of  dark-red  color.  Besides  these  large  grooves, 
there  are  smaller  ones,  which  give  a  coarsely  granular 
appearance  to  the  surface.  The  thickness  of  the  cortex 
is  very  uneven;  at  one  place  it  may  be  normal,  while 
at  another  it  is  very  much  thinner;  the  characteristic 
outline  of  the  parenchyma  is  well  preserved  at  the  nor- 
mal places.  The  rigidity  of  the  thickened  arterial  walls 
is  a  constant  feature  in  the  arterio-sclerotic  shrunken 


30 


kidney.  The  uneven  thickening  of  the  walls  is_  es- 
pecially pronounced  in  the  arterial  branches  which  lie  in 
the  broadest  and  deepest  grooves  of  the  surface  of  the 
corresponding  part  of  the  parenchyma. 

The  high-grade  atheromatous,  arterial  changes,  which 
are  sometimes  fohowed  by  a  complete  obliteration  of 
the  lumen,  are  especially  conspicuous  under  the 
microscope.  The  histological  peculiarities  _  of  the 
atrophic,  parenchymatous  changes  are  very  similar  to 
those  of  the  senile  kidney  atrophy.  Here  and  there  is 
regularly  observed  the  destruction  of  the  malphigian 
tufts,  whereby  these  often  become  the  seat  of  a  calcifica- 
tion;' here  and  there  the  epithelium^  of  the  uriniferous 
tubules  becomes  smaller,  flatter,  more  uniform,  and 
color  more  intensely,  whereby  the  uriniferous  tubules 
suffer  a  narrowing  before,  finally,  here  and  there,  col- 
lapsing completely.  The  difference  between  the  his- 
tological changes  of  the  simple  senile  atrophy  of  the 
kidney  and  the  arterio-sclerotic  shrunken  kidney  con- 
sists in  the  different  localization  and  intensity  of  the 
disease  processes.  While  these  occur  more  diffusely,  and 
are  quite  insignificant  in  the  senile  kidney,  they  occur  in 
groups  in  the  arterio-sclerotic  kidney,  and  reach  a  much 
higher  degree.  It  seems,  for  this  reason,  that  there  is 
an^  increase  in  the  interstitial  connective  tissue  in  the 
vicinity  of  the  atrophic  foci  in  the  arterio-sclerotic  kid- 
ney. This,  however,  is  only  apparently  so,  and  is  due 
to  the  collapse  of  the  uriniferous  tubules,  because  in 
the  pure  forms  of  arterio-sclerotic  shrunken  kidney 
there  is  really  no  proliferation  or  hyperplasia  taking 
place. 

A  different  picture  appears  when,  in  addition  to  the 
simple  atrophic  processes  in  the  arterio-sclerotic 
shrunken  kidney,  there  really  is  a  proliferation  of  the 
interstitial  connective  tissue.  In  such  cases  the  dif- 
ferential diagnosis  between  the  arterio-sclerotic  kidney 
and  some  forms  of  the  inflammatory  shrinkage  is  rather 
difhcult.  Such  kidneys  only  are  to  be  regarded  as 
arterio-sclerotic  in  which  the  changes  in  the  uriniferous 
tubules  are  evident,  and  where  the  proliferatipn  of  the 
connective  tissue  is  insignificant  and  is  exclusively  con- 
nected with  the  atrophic  foci.  A  high-grade  hyper- 
plastic   involvement    of     the     inter-tubular    connective 


31 


tissue,  a  marked  thickening  of  the  capsule  of  the  glom- 
eruli, numerous  and  extensive  round-cell  infiltrations, 
and  finally  necrosis  and  desquamation  of  the  epithelium 
of  the  uriniferous  tubules,  all  these  must  be  regarded  as 
symptoms  only  of  a  different  condition,  namely,  the 
inflammatory  shrunken  kidney.  The  changes  which 
are  seen  with  the  naked  eye  are  not  sufificient  for 
a  differential  diagnosis.  The  extent  and  intensity  of  the 
changes  in  the  vessels  must  be  treated  very  carefully, 
therefore,  when  considering  the  verified  observations 
on  the  great  arterial  branches.  One  must  not  for- 
get that  the  vessels  which  lie  within  the  chronic- 
ally inflamed  kidney  may  suffer  a  thickening  of  their 
walls  and  a  narrowing  of  their  lumen,  and  even  an 
obliteration,  due  to  a  proliferation  in  the  intima. 

For  this  reason  I  kept  in  mind,  during  my  investiga- 
tion of  the  diagnosis  of  the  arterio-sclerotic  shrunken 
kidney,  the  short  but  excellent  remark  of  Orth  (310, 
p.  128):  "If  we  find  the  interstitial  tissue  unchanged 
or  only  slightly  changed,  or  changed  in  spots,  then  we 
must  regard  the  change  in  the  vessels  as  primary,  and 
diagnose  it  as  an  arterio-sclerotic  atrophy." 

The  proportion  of  frequency  of  the  arterio-sclerosis, 
the  inflammatory  shrunken  kidney,  the  arterio-sclerotic 
and  the  simple  senile  atrophy  is  illustrated  by  the  fol- 
lowing table  of  1,106  dissections  in  the  pathological 
anatomical  Institute  of  Krakau. 

TABLE  II. 

The  frequency  of  arterial  atheroma  and  kidney  degener- 
ations (exclusive  of  acute  alterations,  amyloid  and  engorged 
kidney)  ace.  to  the  journals  of  the  Pathologico-anatomical 
Institute  Krakau,  of  in  the  year  1895. 


A  GE  PERIOD 


TOTAL 


Nephritis  chronica 

Cirrhosis  from  arteriosclerosis 

Atrophia  senilis  simplex  (no  Albuminurie) 

29 

12 

I 

12 

14 
16 
67 

55 
17 
79 

Sum  of  kidney  degenerations 

29 

25 

97 

151 

32 


Percentage  of  cases 

to  autop 

sies 

AGE     PERIOD 

1-40 

40-30 

50-90 

Generally 

Atheroma    cases 
Nephritis  chronica 
Cirrhosis  from  arteriosclerosis 
Atrophia  senilis  simplex 

I  .eg 
4.00 

22.65 

9-37 
0.78 

9-37 

58.89 

5.53 
6.32 
26.47 

16.82 
4-97 
1-53 
7-14 

Percentage  of  kidney  degenerations  among  each 

other 

AGE     PERIOD 

1—40        40-30 

50-go 

Generally 

Nephritis  chronica 

Cirrhosis  from  arte-iosclerosis 

Atrophia  senilis  simplex 

100 

48 

4 

48 

14-43 
16.39 
69.08 

36.43 
H.26 

52.31 

In  each  one  hundred  dissections  there  are,  therefore: 
cases  of  atheroma,  16.82  per  cent. ;  chronic,  inflamed, 
shrunken  kidney,  4.97  per  cent. ;  arterio-sclerotic  kidneys, 
1.53  per  cent.;  simple  senile  atrophy  of  the  kidney,  7.14 
per  cent.  From  this  table  we  can  draw  the  conclusion 
that  the  kidney  changes  due  to  arterio-sclerosis  are  by  no 
means  frequent.  In  old  people  they  are  surely  found 
much  less  frequently  than  the  simple  senile  atrophy.  In- 
deed, both  of  the  other  forms  of  the  retrogade  disturb- 
ances of  nutrition  of  the  kidney  are  only  found  about 
one-half  as  frequently  as  the  arterio-sclerosis  of  the  ves- 
sels in  the  aged. 

Launois  maintains  on  the  contrary  (72,  p.  17),  that 
atrophy  of  the  kidneys  is  the  rule  in  old  people;  under 
the  microscope  one  finds  constantly  in  all  cases  that:  "II 
s'agit  la  .  .  .  d'une  nephrite  interstitielle,  d'une  sclerose 
renale  (p.  19)."  The  starting  point  of  the  latter  is  again 
regularly  found  in  the  atheromatous  changes  of  the  ves- 
sels (p.  27).  7\lso  Guyon  (comp.  85,  p.  108),  literaUy 
confirm'3  this  statement  of  his  pupil.  Guyon  and  Launois 
maintain  at  the  same  time,  that  the  arterial  sclerosis  and 
its  consequences  are  constantly  to  be  found  in  individuals 
with  hypertrophy  of  the  prostate  gland. 

The  climax  of  the  Guyon  theory  is  the  well-known  sen- 
tence, always  and  everywhere  quoted:  "Sous  les  prosta- 
tiques  sont  atheromateux  {^2,  p.  9-85,  p.  108). 

Hypertrophy  of  the  prostate  is  a  wide-spread  disease 
which,  as  is  well  known,  is  observed  in  every  third  or 
fourth  okl  man.     It  can,  however,  be  seen  from  the  above 


33 


table  of  the  i,io6  dissections,  that  ani'ong  all  the  disease 
processes  forced  by  the  French  school  into  a  nnirorm 
clinical  picture,  the  arterio-sclerosis  is  the  one  most  fre- 
quently observed;  that  is,  on  an  average  in  every  second 
person  a'bove  fifty  years  of  age,  the  prostatic  hyper- 
trophy is  rarer,  and  the  arterio-sclerotic  shrunken  kidney 
is  found  in  only  seven  per  cent,  of  the  aged.  Guyon's 
views  are  therefore  contradicted  by  these  purely  statis- 
tical data.  The  following  facts  speak  still  more  deci- 
sively against  them: 

Among  my  forty-two  cases  of  extensive  arterial  sclero- 
sis there  were  only  ten  cases  in  which  the  renal  vessels 
were  atheromatous.  In  seven  cases  of  arterial  sclerosis 
of  the  nenal  vessels  I  observed  at  the  same  time  hyper- 
trophy of  the  prostate.  The  condition  of  the  kidneys 
may  be  stated  as  follows  (compare  table  I)  :  arterio- 
sclerotic shrunken  kidney  only  once,  inflammatory 
shrunken  kidney  once,  simple  senile  atrophy  of  the  kid- 
ney twice,  infarction-cicatrix  once,  and  finally,  in  two 
cases,  no  pathological  changes  were  found  in  the  kidneys. 

Even  if  we  disregard  the  differing  of  the  arterio-sclero- 
tic shrunken  kidney  and  inflammatory  shrunken  kidney 
from  the  simple  senile  kidney  atrophy,  there  still  remains 
as  a  final  result  of  my  investigation,  that  among  twenty- 
one  cases  of  hypertrophy  of  the  prostate  (in  seven  cases 
concurrent  with  atheroma  of  the  renal  arteries)  the 
changes  in  the  kidneys,  accompanied  by  decrease  in  size, 
were  observed  only  four  times ;  in  the  remaining  seven- 
teen cases  of  hypertrophy  of  the  prostate  the  kidney 
changes  alleged  by  Launois  to  be  constantly  observed 
were  not  found  at  all. 

In  female  individuals  I  found  among  five  cases  of  gen- 
eral arterial  sclerosis  four  cases  of  arterio-sclerotic 
changes  in  the  renal  vessels,  and  among  these  the  arterio- 
sclerotic shrunken  kidney  was  only  observed  once ;  while 
in  the  remaining  three  cases  there  was  only  a  simple 
senile  atrophy. 

In  the  aged  male  I  found,  on  the  other  hand,  among 
forty-two  cases  of  general  or  extensive  arterial  sclerosis 
(of  which  in  ten  cases  the  renal  arteries  also  were 
changed)  the  following  condition  of  the  kidnevs :  simple 
senile  athropy  of  the  kidney  seven  times,  inflamimatorv 
shrinkage   two  times,   chronic   inflammation   of   the   kid- 


34 


ney  without  shrinkag'e  one  time,  arterio-sclerotic  shrunk- 
en kidney  four  times. 

Among  the  latter  four  cases  the  prostatic  gland — what 
I  consider  necessary  again  to  lay  stress  upon — was  only 
once  enlarged,  and  that  only  to  a  small  degree.  (Weight, 
25  g. ;  case  2.)  In  two  other  cases  the  prostate  gland  was 
of  normal  size  and  weight  (case  28  and  40)  ;  in  the  fourth 
case  (20)  it  was  'even  smaller,  atrophic  (weight,  12  g.). 
Besides  this,  I  found,  in  the  forty-two  cases  mentioned, 
the  following  pathological  changes  in  the  kidneys  : 
Acute  inflammation  of  the  kidney.  ...      3  times 

Infarction  citrix  of  the  kidney 2  times 

Pyelitis  calciilosa  of  the  kidney i   time 

Amyloid  deg-eneration  of  the  kidney,      i   time 
Cystic  degeneration  of  the  kidney.  ...      1   time 
Passive  hypersemia  of  the  kidney.  ...      2  times 
In  the  remaining  18,  that  is  to  say,  in  nearly  one-half 
of  my  cases,  there  were  neither  macro  nor  microscopical 
pathological  changes  to  be  observed  in  the  kidneys.    In- 
deed, among  these  18  cases,  there  were  only  2  in  which 
the  existence  of  the  arterio-sclerotic  changes  could  be 
demonstrated  in  the  proximal  end  of  the  main  branches 
of  the  renal  arteries. 

In  consideration  of  these  facts  one  is  fully  justified  in 
asking,  upon  what  does  the  Guyon  school  support  its 
assertion,  that  changes  in  all  the  genito-urinary  organs 
appear  synchronously,  are  similar  everywhere,  and  are 
everywhere  produced  by  arterio-sclerosis?  One  remem- 
bers involuntarily  the  remark  of  Charcot  (190): 

"Dans  la  vieillesse,  les  organes  semblent  rester  en 
quelque  (sorte  independants  les  uns  des  autres ;  ils  souf- 
frent  isolement  et  les),  diverses  lesions  dont  ils  peuvent 
devenir  le  siege  ne  ressentissent  guere  sur  I'ensemble  de 
I'economie." 


35 


CHAPTER  V. 

RELATION     OF    THE    ARTERIAL    ATHERCflA    TO 
THE     BLADDER 

As  may  be  judged  from  the  preceding  chapter  I  have 
drawn  the  conclusion  that  the  Guyon  theory  with  regard 
to  the  prostate  and  the  kidney  cannot  sustain  a  serious 
criticism,  and  therefore  must  fall  to  the  ground. 

Notwithstanding  this,  it  seemed  to  me  necessary  that 
the  significance  of  the  arterial  sclerosis  as  affecting  the 
bladder  should  be  given  a  thorough  examination ; 
because  it  might  be  possible  that  arterial  sclerosis  of 
the  bladder  vessels  should  exist  entirely  independently 
of  a  concurrent  atheroma  of  the  other  vessels,  and  ex- 
ercise an  injurious  influence  upon  the  condition  and  ef- 
ficacy of  the  muscles  of  the  bladder. 

This  possibility  might  explain  the  puzzling  bladder 
weakness  in  old  people. 

The  question  then  arises  whether,  in  the  cases  under 
consideration,  such  anatomical  changes  in  the  bladder 
muscles  can  be  proven,  and  whether  these  changes  would 
sufficiently  explain  the  possibility  of  bladder  insufficiency 
being  due  to  arterial  sclerosis.  The  answer  to  this  ques- 
tion is  by  no  means  easy;  mainly  because  we  have 
here  to  deal  with  a  relative,  numerical  proportion,  and 
next  with  a  comparison  of  the  strength  of  the  bladder 
muscles  to  that  of  the  inter-  and  intra-muscular  con- 
nective tissue;  and  in  addition  we  must  make  sure  of 
the  proportion  between  the  alleged  structural  changes 
within  the  bladder  wall  and  the  manifest  arterio-sclerotic 
processes  in  the  smallest  intra-parietal  arteries. 

Before  the  appearance  of  the  works  of  the  Parisian 
school,  hardly  anvbody  had  ever  made  an  attempt  to 
search  for  an  anatomical  basis  for  bladder  nisufificiency. 

36 


It  was  considered  enough  to  look  upon  the  oibserved 
bladder  insufficiency.     Whether  spontaneous  or  due  to 
a  hypertroiphy  of  the  prostate,  as  a  disease  produced  by 
.  "Paresis,"  "Atony/'  "Weakening,"  etc. 

First,  so  far  as  I  know,  in  1872  Dittel  (24)  called 
attention  to  the  fatty  degeneration  of  the  bladder  mus- 
cles as  a  cause  of  senile  bladder  insufficiency.  A  few 
years  later,  in  1881,  we  find  a  short  remark  by  Maas 
(84  p.  522),  in  which  he  pointed  out  the  fatty  degen- 
eration of  the  hypertrophic  muscles  of  the  bladder  as  a 
cause  of  the  rarely  observed  rupture  of  the  bladder. 

This  statement  of  Maas  found  a  place  in  the  major- 
ity of  the  text-fbooks  and  manuals  of  surgery. 

Now  and  then  the  colloid  degener?tion  of  the  muscle 
bundles,  as  first  demonstrated  b_v  Rokitansky  (112),  was 
mentioned  as  supposed  to  lessen  the  conitractility  of 
the  bladder  (Kautschukblase). 

Bohdanowicz  (7)  does  not  mention  the  fatty  degenera- 
tion of  the  muscle  cells  ("Degeneratio  adiposa").  He 
occupied  himself  inore  with  the  distributio'n  of  the  true 
fat  tissue  in  the  bladder  wall. 

In  young  and  healthy  individuals  one  should  find  small 
collections  of  true  fat  tissue  exclusively  in  the  sub- 
serous connective  tissue  layer  of  the  bladder  wall,  and 
in  proportion  to  the  general  condition  of  nutrition.  In 
the  fibrous  degeneration  of  the  bladder  wall  (sclerotic), 
which  is  often  seen  in  muscle  hypertrophy,  the  fat  tis- 
sue is  in  a  preponderance.  Not  only  is  it  found  in  the 
subserous  layer,  but  it  also  extends  from  this  into  the 
external  muscle  bundles.  In  the  highest  degree  of  these 
changes  fat  is  seen  in  places  where  it  is  never  found  in 
normal  individuals;  that  is,  between  the  muscle  bundles 
of  the  innermost  layers  and  even  in  the  sub-mucous 
membrane. 

This  pathological  increase  of  fat  tissue  (to  which,  in 
my  opinioTi,  the  name  "Lipomatosis"  'belongs)  bas 
nothing  in  common  with  the  physiological  collection  of 
fat  tissue,  but  is  a  symptom  independent  of  the  nutritive 
condition  of  the  individual  and  co-ordinated  with  the 
sclerosis  of  the  bladder  wall. 

In  a  part  of  my  cases  I  had  to  refrain  from  the 
microscopical  examination  of  the  material  in  a  fresh 
condition   (frozen   section)   as  well  as   from   fixation   of 

37 


the  pieces  in  mixtures  of  osmic  acid.  For  this  reason  I 
am  not  justified  in  making  a  definite  statement  with 
regard  to  the  true  fatty  degeneration  of  the  muscle- 
cells  mentioned  by  Dittel  and  Maas  (Degeneratio  adi- 
posa).  Still,  it  seems  to  me  that  the  true  fatty  degen- 
eration of  the  bladder  muscles  is  not  a  very  frequent 
and,  where  it  really  exists,  not  a  very  extensive  phenom- 
enon; at  least,  this  seems  to  be  proven  by  those  of  my 
cases  which  were  thoroughly  examined  for  it.  It  is 
b}'  no  means  denied  that  such  changes  do  occur,  and 
that  they  occur  in  cases  in  whic'h  the  bladder  wall  has 
an  extraordinary  friability.  The  number  of  such  cases 
cannot  possibly  be  great,  because  I  never  encountered 
such  friable  bladder  walls  in  any  of  my  cases. 

Besides,  it  seems  probable  that  prev  iling  severe  in- 
flammatory processes  must  be  held  responsible  for  the 
possibility  of  the  occurrence  of  such  bladder  walls. 
Such  inflammatory  processes  of  the  bladder  must  be 
looked  upon  as  accidental  complications,  which  over- 
step the  limits  of  the  conception  of  a  spontaneous 
simple  bladder  insufficiency. 

Be  it  as  it  may,  one  thing  is  certain  rbove  all  doubt; 
that  is,  that  the  cause  of  bladder  insui^ciency  in  old 
people  is  certainly  not  to  be  sought  in  the  fatty  degen- 
eration of  the  bladder  muscle,  because,  if  this  were  so, 
the  fatty  degeneration  must  appear  in  all  cases,  and  in 
the  great  majority  of  muscle  cells. 

Much  less  can  a  colloid  degeneration  of  the  muscle 
cells  be  looked  upon  as  of  causative  significance  with 
regard  to  bladder  insufficiency. 

These  changes  are  sometimes  met  with  in  very  pro- 
tracted inflammatory  processes  of  the  urinary  bladder, 
in  which  the  walls  have  lost  their  elasticity.  But  such 
urinary  bladders  I  have  intentionally  excluded  from  my 
investigation  because  of  their  inflammatory  complica- 
tions. 

But  Bohdanowicz's  statement,  too,  I  can  by  no  means 
verify. 

I  have  in  every  case  paid  particular  attention  to  the 
changes  described  by  him,  and  I  came  to  the  conclusion 
that  the  quantity  and  localization,  as  well  as  the 
presence  of  true  fat  tissue  within  the  bladder  wall,  is  in 
direct    proportion    to    the    nutrition    of    the    individual. 

38 


The  better  the  nutrition  and  the  richer  the  layer  of  fat 
of  the  epidermis,  the  more  frequent  and  the  richer  are 
the  fat  tissue  collections  in  the  muscles  of  the  urinary 
bladder.  For  this  reason  one  is  not  justified,  in  my 
opinion,  in  paying  much  attention,  to  the  increase  of 
fat  tissue  in  the  bladder  wall.  This  Lipomatosis  is  a 
phenomenon  which  has  no  intimate  relationship  to  the 
pathological  conditions  of  the  bladder  wall. 

In  a  few  cases  in  which  a  microscopic  investigation 
of  the  hypertrop-hic  bladder-wall  was  carried  on  prior  to 
1884  little  attention  was  paid  to  the  condition  of  the  in- 
terstitial connective  tissue  o-f  the  'bladder-wall. 

Nothing  can  be  gathered  from  either  the  work  ol  Jean 
(62)  or  that  of  Robelin  (109). 

In  Germany  Maas  only  (84,  p.  521)  mentions — and  he 
but  briefly — the  thickening  of  the  mucosa  and  submucosa 
in  hypertrophy  of  the  bladder  and  in  catarrh  of  the 
bladder;  and  Orth  (310)  mentions  the  occurring  atrophy 
of  the  muscles  in  certain  cases  of  protracted  dilatation  of 
bladder  (1.  c.  p.  220). 

Launois  {'/2)  was  the  first  one  who  considered  this 
question  more  in  detail.  He  maintains  that  by  the 
working  hypertrophy  of  the  bladder  muscles  occurring  in 
consequence  of  prostatic  hypertrophy,  "les  elements  con- 
tractiles  .  .  .  se  trouvent  englobes  dans  une  gaine 
de  tissu  conjonctif  dense  et  serre,  qui  gene  d'abord  leur 
action  et  qui,  par  son  developpemient,  la  supprime  com- 
pletement"  (1.  c.  p.  51).  The  miain  cause  of  this  con- 
nective tissue  proliferation,  which  occurs  actively  in  these 
sclerotic  processes,  is  always  to  be  found  in  the  athero- 
matous, degenerated  arteries. 

To  this  "sclerosis"  of  the  bladder-wall  we  'have  to  refer 
the  forms  of  bladder  insufficiency  which  are  spontaneous, 
i.  e.,  occurring  without  prostatic  hypertrophy.  Still 
greater  stress  is  laid  upon  these  assertions  in  the  numer- 
ous works  o'f  Guy  on  (40,  41,  44,  46). 

All  clinical  manifestations  of  the  so-called  "proistatis- 
mus"  could,  as  he  maintains  (45),  occur,  not  only  in  old 
people  w'ho  are  not  suiTering  fro;m  prostatic  hypertrophy, 
but  also  in  females,  provided  that  there  were  a  pre-exist- 
ing sclerosis  of  the  bladder-wall  produced  by  the  arterial 
sclerosis.  As  proof  of  this  can  be  cited  a  few  cases 
puljlis-hcd  l)y  Guyon's  pupils;  as,  for  instance,  Recaaiiier's 


39 


case  (ii6  "P'rostatisme  vesical"  in  a  40-year-old  man),  or 
the  case  of  Ohevalier  (17).  A  proof  of  the  same  is  in  the 
case  of  a  woman  43  years  of  age  who  (what  deserves 
mention)  had  passed  through  a  persistent  and  protracted 
inflammation  of  the  bladder,  and  who  was  examined  only 
during"  her  lifetime.* 

In  other  works  published  by  the  pupils  of  Guyon,  as 
for  instance  in  that  by  Desnos  (27),  as  well  as  in  the  Ger- 
man compilations  and  essays  of  Mendelsohn  (97),  and 
Giiterbock  (50,  51),  and  in  a  treatise  of  Assmuth  (4  two 
microscopically  examined  cases),  as  well  as  in  the  Polish 
compilation  of  Misiewicz  (86),  etc.,  nothing  essentially 
new  is  to  be  found. 

The  statements  of  the  Parisian  school  and  its  followers 
were  first  attacked  by  Casper  (16).  His  investigations 
concerning  the  fibrous  degeneration  of  the  bladder-wall 
were  not  finished  when  his  work  was  published,  and  a 
later  publication  of  it  is  not  known  to  me.  However,  on 
account  of  the  fact  that  he  found  atheromata  in  the  small 
arteries  of  the  bladder  only  8  times  among  24  cases  of 
prostatic  hypertrophy  with  arterial  sclerosis,  Caspar  be- 
lieves that  he  may  draw  the  following  negative  conclu- 
sion: "Therefore  the  explanation  remains  .  .  .  still 
hypothetical  for  the  cases  considered  of  dysuria  and  the 
atrophy  related  to  degeneration  of  the  bladder  muscles." 

The  puzzling  occurrence  of  the  functional  power  of  the 
bladder  which  lately  was  observed  in  certain  cases  of 
prostatic  hypertrophy  after  castration  seems  not  only  to 
strengthen  the  doubt,  especially  brought  to  notice  by 
Caspar,  but  points  to  the  conclusion  that  in  these  cases 
in  question  the  bladder  muscle  did  not  suffer  at  all  from 
a  retrograde  disturbance  of  nutrition,  be  it  atrophy  or 
perhaps  a  degeneration  (vide  Frisch,  379). 

Bo'hdanowicz  (7)  is  in  complete  accord  with  Caspar  in 
the  belief  that  the  arterial  sclerosis  is  of  no  great  im- 
portance for  the  condition  of  the  bladder-wall,  but  yet  he 
takes  it  as  proven  that  the  "sclerosis"  of  the  bladder 
muscles  exists.  He  believes  that  it  is  not  necessary  to 
search  ihere  for  another  cause,  as  the  overworking  "sur- 


*In  this  place  a  work  by  Croom  (18)  deserves  mention.  In 
It  he  rightly  pointed  out  that  the  difficulty  of  urination  in 
women  is  mostly  a  consequence  of  a  disease  process,  not  oc- 
curring in  the  urinary  apparatus  itself,  but  in  its  neighborhooa 


40 


menage"  in  the  first  place  has  a  muscle  hypertrophy  as 
a  consequence,  and  later  often  produces  a  state  of 
sclerotic  degeneration.  (1.  c.  p.  68.)  Bolidanowicz 
makes  the  hypothesis  that  the  fibrous  degeneration  of  the 
bladder-wall  occurs  only  when  the  bladder  muscles  cease 
tO'  be  hypertrophied. 

Bohdanowicz  does  not  furnish  sufificient  explanation,  in 
the  connection  of  the  fibrous  degeneration  of  the  bladder- 
wall  with  the  muscle  hypertrophy,  for  thiose  cases  in 
which,  besides  a  bladder  insufficiency,  no  changes  could 
be  proven  which  would  be  capable  of  causing  a  bladder 
hypertrophy. 

Among  the  cases  investigated  by  Bohdanowicz,  one 
of  so-called  "prostatisme  vesical"  is  found  (No.  xxi.), 
in  which  a  fibrous  degeneration  of  the  bladder  wall  was 
confirmed,  in  addition  to  a  general  sclerosis. 

The  result  of  the  investigation  of  this  case  was 
summed  up  in  the  following  way:  "La  vessie 
(scleroisee),  que  I'on  pourrait  attribuer  a  un  vieux  pros- 
tatique  atheromateux,  suivant  les  idees  regnantes." 

But  I  must  here  call  attention  to  one  circumst  mce, 
in  my  opinion,  important;  namely,  in  this  case  cited 
there  existed  for  years  a  chronic  suppurative  inflamma- 
tion of  the  bladder,  and  the  microscopical  examination 
proved  that  there  existed  a  high-grade  sclerotic  change 
in  the  neighboThood  of  the  muscle  layer  next  to  the 
mucosa.  One  cannot,  therefore,  disregard  the  thought 
that  in  this  case  the  bladder  inflammation  was  primary, 
and  that  the  fibrous  degeneration  of  the  bladder,  ex- 
tending fromi  within  outward,  was  a  secondary  symp- 
tom caused  by  the  bladder  inflammation. 

Finally  Miquet  (87)  has  concerned  himself  with  these 
questions;  but  his  thesis  is  almost  solely  a  compilation  of 
the  previously  published  facts. 

Against  all  cited  investigations  of  the  influence  of  the 
arterio-sclerosis  upon  the  condition  of  the  bladder  mus- 
cle we  must  make  a  double  objection.  Firstly,  only 
such  cases  as  were  obscured  by  an  already  extensive 
inflammatory  complication  were  used  in  all  these  investi- 
gations. 

These  cases  should  have  been  put  aside,  because  a 
chronic  inflammatory  process  is  regularly  followed  by  a 
fibrous  degreneration  of  the  submucosa. 


41 


I  can  maintain  that  the  latter  is  really  the  case  on 
the  evidence  of  a  few  cases  cited  in  this  work,  as  well  as 
of  a  few  cases  which  have  not  been  considered  here. 

It  is  also  easy  to  convince  one's  self  of  the  fact,  in 
cases  of  chronic  infiammation  of  the  bladder  in  young 
female  individuals,  that  the  fibrous  degeneration  pro- 
duced by  inflammatory  irritation,  progresses  more  ex- 
tensively in  time,  till,  finally,  after  years  of  persisting 
bladder  catarrh,  it  involves  the  whole  thickness  of  the 
wall.  In  such  cases,  in  which  we  of  course  cannot 
speak  of  the  influence  of  the  arterial  sclerosis,  nor  of 
the  effects  produced  by  obstruction  to  micturition — in 
which  there  was  not  even  the  least  hypertrophy  of  the 
bladder  muscles — in  such  cases  the  fibrous  degeneration 
of  the  bladder  wall  can  only  be  considered  as  being 
due  to  the   efl^ect   of  a  chronic  inflammatory  irritation. 

As  a  proof  of  this  statement,  the  distribution  of  the 
sclerotic  changes  may  also  be  easily  ascertained.  Here 
the  fibrous  degeneration  is  undoubtedly  produced  by 
an  active  connective  tissue  proliferation.  This  is 
proven  by  the  circumstance  that  the  bladder  wall  in 
these  cases  shows  a  high  degree  of  thickening.  Al- 
though, as  I  had  an  opportunity  to  prove  to  myself  by 
microscopical  measurements,  the  muscles  showed  no 
hypertrophy  worth  mentioning,  the  mode  of  origin  of 
the  fibrous  degeneration  pointed,  on  the  other  hand, 
to  the  presence  of  inflammatory  round-cell  infiltration 
wdthin  the  thickened  connective  tissue  bands. 

It  seems,  therefore,  not  admissible  to  draw  any  con- 
chisions  from  the  superficial  histological  investigation  of 
the  condition  of  the  bladder  w?ll  in  cases  of  bladder 
insufficiency  of  old  people  complicated  with  inflamma- 
tory processes,  because  it  is  impossible  to  decide  in  such 
cases  whether  the  condition  of  the  bladder  wall  is  a 
consequence  of  the  afore-mentioned  inflammatorv  com- 
plications or  whether  it  is  a  consequence  of  still  other 
causes. 

This  claim  holds  good  also  for  those  cases  of  blad- 
der insufficiency  produced  by  prostatic  hypertrophy  as 
well  as  for  the  "spontaneous"  cases  to  which  the  name 
"prostatisme  vesical"  is  given.  For  this  reason  we  can- 
not make  use  of  the  cases  of  Bohdanowicz  before  men- 
tioned,  nor  of  other   similar  ones,   when   we  deal   with 


42 


the  explanation  of  the  question  where  to  search  for 
the  cause  of  "spontaneous"  'bladder  insufftciency. 

The  second  deficiency  which  was  noticed,  in  the 
works  referred  to  above,  may  be  summed  up  in  this: 
The  decision  of  all  investigators  was  based  upon  a  very 
superficial  estimation  of  the  strength  of  the  bladder 
muscles  and  of  the  interstitial  connective  tissue.  But 
it  is  also  well  known  how  difficult  it  is  to  avoid  gross 
mistakes  if  one  does  not  resort  to  micrometric  measure- 
ments. Although  such  measurements  are  not  sufficient 
to  eliminate  all  sources  of  mistakes,  they  are  sufficient 
to  reduce  the  number  of  these  mistakes. 

In  my  investigation  forty  bladders  of  old  men  were 
utilized.  All  of  them  had  been  attacked  by  arterio- 
sclerosis and  in  about  one-half  (nineteen  times)  there 
was  at  the  same  time  a  prostatic  hypertrophy.  Besides 
these,  I  examined  five  urinary  bladders  of  old  female 
individuals  with  high-grade  and  extensive  arterial 
sclerosis,  and,  finally,  for  comparison,  eleven  bladders 
of  young  men,  in  which  there  were  no  changes  in  the 
arterial  system  or  in  the  prostate  glands. 

In  all  cases  I  tried  to  determine  as  accurately  as  pos- 
sible with  the  micrometer  the  relation  of  the  bladder 
muscle  to  the  interstitial  connective  tissue  of  the  bladder 
wall.  To  be  absolutely  correct  one  should  compute  the 
relation  between  these  two  components  of  the  bladder 
wall  in  cubic  units.  This,  however,  cannot  be  carried 
out,  for  the  reason  that  the  microscope  gives  us  only 
two  dimensions  lying  in  one  plane.  But  I  have  also 
refrained  from  the  calculation  in  quadratic  units;  first 
for  want  of  suitable  measuring  instruments,  and  sec- 
ondly, because  the  linear  measurements  of  the  thickness 
of  the  bladder  wall  seemed  to  be  sufficient  for  my  pur- 
pose. I  was  soon  convinced  of  the  fact  that  the  main 
connective  tissue  bands  in  which  the  quantitative 
changes  are  first  apparent  run  exclusively  longitud- 
inally. If  one,  therefore,  measures  the  transverse  di- 
mensions (in  the  microscopic  preparation  the  vertical) 
of  these  main  connective  tissue  bands,  data  will  be  ob- 
tained which  are  entirely  sufficient  to  measure  the  de- 
gree of  thickening  of  these  bands.  The  narrow  con- 
nective tissue  bands  which  stand  vertically  to  the 
surface  of  the  mucous  membrane,  running  respectively 


43 


obliquely,  can  be  left  out  without  great  consequence, 
because  their  thickening  never  reaches  a  considerable 
degree.  I  paid  attention  especially  to  investigating  how 
the  interstitial  connective  tissue  is  made  up;  whether  it 
is  loose  or  dense  or  compact.  I  also  paid  attention  to 
the  behaviotr  of  the  smaller  interfascicular  and  inter- 
fibrillar  connective  tissue  septa.  The  linear  measure- 
ments were  also  sufficient  for  my  purpose,  because  I, 
in  all  my  comparisons  and  compilations,  made  use  of 
relative  values,  while  I  regarded  the  numerical  value 
of  the  connective  tissue  as  a  unit  of  measure.  Next 
I  computed  the  absolute  thickness  of  all  the  muscular 
layers,  then  the  thickness  of  all  connective  tissue  bands 
which  lay  in  the  direction  of  the  same  straight  line 
which  connected  the  mucous  membrane  with  the  ex- 
ternal surface  of  the  bladder.  These  two  numbers 
were  divided  by  each  other,  and  the  quotient  showed 
how  many  times  the  muscles  are  thicker  than  the  con- 
nective tissue.  We  can  also  represent  this  relationship 
in  the  form  of  a  proportion: 

Connective  tissue  i 


Muscle  X 

The  hypertrophy  as  well  as  the  atrophy  of  the  muscle 
is  in  the  first  place  expressed  in  the  thickness  of  the 
muscular  bundles.  The  more  the  muscle  develops  in 
proportion  to  the  interstitial  connective  tissue,  the 
greater  will  be  the  difference  in  the  thickness  of  the 
muscle  bundles  and  the  connective  tissue,  and  the 
greater  will  be  the  x  of  our  proportion. 

Of  course  it  is  impossible  on  the  basis  of  these  calcu- 
lation's to  decide  whether  there  is  a  true  hypertrophy  of 
the  muscle,  or  wlhether  there  really  is  an  increase  in  the 
interstitial  connective  tissue.  In  this  connection  I  must 
point  out  that  I  succeeded  in  demonstrating,  in  a  manner 
to  be  mentioned  later,  the  existence  of  a  true  hypertrophy 
of  the  bladder  muscle.  Moreover,  it  is  not  pertinent  re- 
specting the  function  of  the  bladder  whether  the  muscle 
becomes  a  victim  of  an  atrophy  whereby  the  connective 
tissue  of  the  bladder  wall  is  relatively  increased,  or  again, 
whether  the  connective  tissire  undergoes  active  prolifera- 

.  44 


tion  and  increase  whereby  the  bladder  muscle,  ciuantita- 
tively  unchanged  or  even  hypertrophied  is  rendered  rela- 
tively less. 

In  both  cases  the  number  of  the  contractile  elements  be- 
com/es  smaller  in  a  given  cubic  unit,  and  the  working  ca- 
pacity of  the  section  of  the  wall  under  consideration  must 
of  course  suffer  an  encroachment.  Even  if  this  be  not 
the  case,  the  functional  final  result  remains  one  and  the 
same :  through  the  atrophy  of  the  muscles  for  wanit  of 
contractile  elements,  and  throtigh  the  active  proliferation 
of  the  connective  tissue  on  account  of  the  preponderance 
of  the  brittle,  unyielding  wall  elements.  The  first  case  is 
not  in  need  of  a  further  explanation ;  as  a  striking  illus- 
tration of  the  latter  possi'bility  one  can  notice  those  brit- 
tle non-comtractile  urinary  bladders  which  are  often  ob- 
served in  chronic  inflammation.  I  have  intentionally  left 
tmconsidered  the  mucous  membrane,  the  submucosa  and 
the  subserosa  in  the  mensuration  of  the  component  parts 
of  the  bladder,  because,  as  already  mentioned,  they  suf- 
fer a  thickening  in  mild  chronic  inflammatory  processes. 
The  thickness  of  the  subserosa  and  of  the  connective  and 
adipose  tissue  on  the  external  surface  of  the  bladder  re- 
spectively ranges  very  much  in  different  individuals  and 
in  different  parts  of  the  bladder  wall.  That  I  might 
utilize  for  comparison  the  degree  of  atheromatous 
changes  in  the  arteries,  I  was  compelled  to  resort  to 
relative  numerical  values  to  establish,  once  for  all,  a 
common  unit.  As  such  a  unit  I  took,  on  the  one  hand, 
the  thickness  of  the  intima,  to  which  I  compared  the 
thickness  of  the  muscularis  and  adventitia;  and,  on  the 
other,  I  took  the  lumen  of  the  vessels,  to  which  I  com- 
pared the  thickness  of  the  walls.  By  these  means  the 
results  of  the  measurements  are  represented  in  the  form 
of  the  following  equations : 

I.     I,  Intima  i,  i 


2,  Media  ^=  2,  x 


3,  Adventitia  3,  y 
II.     Lumen  diameter         i 


Wall  thickness 
45 


These  two  different  units  were  taken  because  some  in- 
vestigators denied  the  existence  of  a  narrowing  of  the 
lumen  produced  by  atheromatosis  of  the  small  arteries. 
Although  I  observed  exactly  the  opposite,  yet,  to  pre- 
vent all  objections,  I  will  for  the  present  leave  this 
question  undecided.  It  seems  almost  unnecessary  to  add 
that  in  each  individual  case  numerous  measurements 
of  numerous  preparations  were  made  of  all  the  arteries 
which  were  cut  longitudinally;  also  that  the  calcula- 
tion of  the  proportions  of  the  components  of  the  bladder 
wall,  the  different  layers  of  the  arterial  walls,  the  wall 
thickness  and  lumen  respectively,  was  executed  sepa- 
rately in  different  places  in  every  individual  case;  and 
finally  that  all  comparisons  were  made  on  a  basis  of 
average  numbers. 

For  the  investigation  only  cases  of  high-grade  and 
extensive  arterio-sclerosis  in  male  and  female  individuals 
were  made  use  of.  From  the  numerous  collection  of 
normal  bladders  only  those  were  used  in  which  there 
was  nothing  which  could  influence  the  accuracy  of  the 
investigation. 

All  cases  in  which  there  was  any  inflammatory  com- 
plication within  the  genito-urinary  system,  and  especially 
withm  the  bladder  wall,  were  excluded.  Exceptionally 
only  I  took  up  a  few  cases  which  might  serve  in  the 
shape  of  examples  to  elucidate  sonie  question,  or  which 
offered  a  particularly  interesting  find  regarding  the 
prostate  gland.  As  I  desired  to  examine  the  begin- 
ning stages  of  the  processes  consequent  to  a  so-called 
prostatic  hvpertrophy,  I  intentionally  excluded  all  those 
cases  in  which  the  enlargement  of  the  prostate  reached 
a  higher  degree  (weight  of  the  prostate  over  50  grams). 

It  is  interesting  to  note  that  it  was  found  that  the  pro- 
portion between  the  two  components  of  the  bladder  wall, 
namely,  the  muscle  and  the  connective  tissue,  undergoes 
rather  great  individual  fluctuation.  Thus  we  meet  cases 
in  which  the  connective  tissue  is  very  scanty  and  the  mus- 
cle tissue  very  abundant  in  the  bladder  wall,  and  vice 
versa,  or  the  connective  tissue  may  quantitatively  equal 
the  muscle  tissue.  The  extreme  proportion  may  be 
expressed  by  the  following  equation: 

46 


Connective  tissue  i 

— —  =  —  as  minimum 


muscle  4 

Connective  tissue         i 

=  —  as  maximum 

muscle  1.2 

Between  these  two  extremes  lie  all  the  other  cases. 

In  this  place,  it  may  be  mentioned  that,  according 
to  Bohdanowicz  (1.  c.  p.  i8),  in  the  normal  urinary 
bladder  the  mucous  membrane  with  the  submucosa  rep- 
resents 2-IO,  the  intermuscular  connective  tissue  2-10, 
and  the  entire  muscle-layer  6-io  of  the  thickness  of  the 
wall.  The  numerical  proportion  of  the  main  component 
parts  of  the  bladder  wall  (without  mucosa,  submucosa 
and  subserosa),  according  to  the  statement  of  this  au- 
thor, is  as  I  ;3.  My  micrometric  investigations  coincide 
entirely  with  the  latter  statement;  that  is,  I  found  in 
the  normal  bladder  the  proportions  fon  an  average)  i  :2.9 
to  1 :3.2.     (Compare  table  5,  left  half.) 

The  structure  of  the  interstitial  connective  tissue  of  the 
bladder  wall  is  in  different  individuals  just  as  dififerent  as 
its  quantitv.  As  a  rule  it  is  only  in  cases  of  chronic 
cystitis  that  it  is  strikingly  dense  and  compact;  otherwise 
it  does  not  became  more  dense  nor  more  compact  in  its 
quantitative  increase. 

In  case  19,  for  instance,  in  w'liich  a  chronic  bladder 
catarrh  existed,  the  proportion  of  the  connective  tissue  to 
the  muscle  was  i  :t.2,  and  at  the  same  time  the  connective 
tissue  was  more  dense  and  more  compact  than  in  norma) 
bladders.  In  case  47,  in  which,  on  the  other  hand,  no 
signs  of  inflammatory  complications  could  be  found,  and 
in  which  the  proportion  of  the  bladder  wall  components 
was  exactly  like  that  of  case  19,  the  connective  tissue  was 
very  loose  and  apparently  increased. 

In  case  38,  for  instance,  there  was,  with  absence  of  in- 
flammatory complication,  a  proportion  of  the  bladder 
wall  connective  tissue  to  the  muscle  of  1  :2.2.  The  first 
was  only  slightly  increased  in  density,  and  the  behavior 
of  the  connective  tissue  was  similar  also  in  case  39,  w'here 
the  proportion  was  1 :2.2i  a.  s.  f. 

Altho'Ugh  the  distribution  of  the  Connective  tissue  fol- 
lows no  constant  rule,  it  may  be  characterized  for  the 
majority  of  cases  in  the  following  way :  The  longest  and 

47 


thickest  connective  tissue  bands  are  found,  in  the  vicinity 
of  the  stronger  venous  and  arterial  ramifications,  between 
the  muscle  layers,  if  these  be  well  limited  (w.hich  is  not 
always  the  case).  These  strong-  connective  tissue  bands 
should  be  named  "perivascular"  connective  tissue. 
Smaller  connective  tissue  septa  lie  between  the  main 
layers  o'f  the  muscular  bundles,  and  should  be  named 
"interfascicular"  connective  tissue;  finally  between  the 
muscle  fibrilla  lie  very  fine  connective  tissue  septa  (inter- 
fibrillar  connective  tissue),  which  can,  in  normal  bladders, 
only  be  dififerentiated  with  high  magnifying  power  as 
something  independent,  otherwise  not  quite  percepti'ble 
and  only  indicated  by  a  fine,  light  line  or  gap  running 
between  two  related  muscle  cells. 

I  have  already  mentioned  that  the  relative  increase  in 
the  quantity  of  the  connective  tissue  of  the  bladder  wall 
becomes  most  conspicuous  in  the  "perivascular"  con- 
nective tissue  bands.  Less  prominent  is  such  an  increase 
in  quantity  in  the  "interfascicular"  connective  tissue,  al- 
though 'here  also  it  can  be  quite  exactly  estimated  by 
micrometric  measurements  and  used  in  the  final  results 
of  the  mensuration.  On  the  other  hand,  the  relative  in- 
crease of  the  "interfibrillar"  connective  tissue  is  not  aic- 
cessible  for  micrometric  investigation  ;  for  this  reason  the 
condition  of  these  very  fine  "interfibrillar"  connective 
tissue  bands  must  be  explored  separately,  and  tlierefore 
the  estimation  of  their  extension  and  thickness,  respec- 
tively, is  of  course  very  inaccurate. 

In  order  to  gain  a  certain  foothold  (anhaltspunkt),  I 
judged  the  strength  of  the  "interfibrillar"  connective  tis- 
sue by  the  test  whether  I  hsd  to  use  a  strong  or  a  weak 
magnifying  lens  to  make  them  visible.  To  cite  the  ob- 
servations under  consideration  more  in  detail  is  not  nec- 
essary. I  believe  I  can  here  limit  myself  to  the  remark 
that  certain  regularities  in  the  behavior  of  the  different 
parts  of  the  connective  tissue  stroma  can  be  demon- 
strated, namely,  that  the  relative  increase  of  the  con- 
nective tissue  in  the  interfascicular  and  interfibrillar 
bands  is  in  a  pretty  constant  proportion  to  that  of  the 
perivascular  connective  tissue  bands.  In  all  cases  in 
which  the  perivascular  connective  tissue  appeared  to  be 
increased,  there  the  finest  interfibrillar  connective  tissue 
septa  were  easily  visible  with  weak  magnifying  lenses. 

48 


When  the  connective  tissue  within  the  bhdder  wall  was 
very  predominant,  the  interfibrillar  connective  tissue 
could  be  differentiated  with  'the  weakest  lenses  as  some- 
thing independent.  Without  exception  the  co^nnective 
tissue  showed  in  all  places  a  loose  structure;  likewise  in 
those  places  in  which  there  was  an  apparent  extensive  in- 
crease. Once  more  I  lay  stress  upon  the  fact  that  I  saw 
a  pronounced  increase  in  density  in  inflammatory  condi- 
tionis  of  the  bladder  only. 

For  this  reason  alone  I  am  inclined  to  assume  that  the 
preponderance  of  the  connective  tissue  within  the  bladder 
wall  is  only  apparent  in  cases  not  complicated  by  in- 
flammatory processes,  and  that  it  does  not  depend  on  a 
real  increase  of  connective  tissue,  but  on  an,  atrophy  of 
the  bladder  muscle.  A  further  support  for  my  opinion 
will  be  found  in  the  discussion  of  the  question  of  bladder 
hypertrophy.  If  we  then  disregard  the  exceptions  oc- 
curring with  inflammatory  complications,  I  must  deny 
the  existence  of  a  primary  bladder  sclerosis  in  the  sense 
of  the  French  investigators.  At  least  my  investigations 
did  not  furnish  me  wich  proof  of  the  correctness  of  the 
statement,  that  the  changes  in  proportion  of  the  bladder 
muscle  to  the  connective  tissue  in  simple,  uncomplicated 
cases,  were  related  to  active  processes  in  the  connective 
tissue  framework. 

The  observation  of  a  "tissu  conjonctif  dense  et  serre, 
qui  etoufife  les  elements  contractiles,"  as  described  by 
French  investigators,  was  possible  only  in  cases  with 
chronic  bladder  catarrli,  which  of  course  is  the  most  fre- 
quent complication  of  prostatic  hypertrophy. 

On  the  other  hand,  it  is  not  to  be  denied  that  in  some 
cases  of  very  old  individuals  there  occurs  a  conspicuous 
chiange  in  the  reciprocal  proportion  of  the  coimponenits 
of  the  bladder  wall  at  the  expense  of  the  muscle,  and  in 
favor  of  the  connective  tissue  framework.  Now  the 
question  is  whether  this  change  can  be  esteemed  as  the 
real  anatomical  basis  for  bladder  insufficiency  in  old  peo- 
ple, and  whether  it  is  sufficient  to  explain  the  clinical 
symptoms? 

A  priori  it  seems  as  if  this  question  can  be  answered 
in  the  affirmative.  The  relative  decrease  of.  the  contrac- 
tile elements,  in  whatever  way  it  may  be  produced,  must 
necessarily  cause  a  decrease  in  the  functional  power  of 

49 


the  involved  muscular  organs.  The  true  relationship  of 
bladder  insufficiency  to  the  decrease  of  the  muscle  can 
then  only  be  assumed  as  proven,  if  we  prove  that  the  in- 
tensity of  the  clinical  phenomena  actually  coincides  with 
the  intensity  of  the  anatomical  changes. 

This  proof  is  supplied  by  a  few  of  my  cases,  namely 
those  in  which  there  existed  duringlife  symptoms  of  blad- 
der insufficiency  (i),  and  in  which  it  was  verified  by 
micrometric  measurements  that  the  proportion  of  the  blad- 
der wall  connective  tissue  to  the  bladder  muscle  did  not 
exceed  i  :2.3.  In  the  history  of  case  six,  for  instance, 
there  was  noted  only  only  a  mild  disturbance  in  the  ex- 
cretion of  urine,  which  nearly  corresponded  to  the  so- 
called  "first  stage"  of  Guyon's  prostatism-us ;  the  propor- 
tion of  the  components  of  the  posterior  wall  of  the  blad- 
der (containing  340  c.c.  of  urine)  was  in  this  case  i  :2.3. 
In  case  44,  an  old  female  individual,  who  suffered  from  a 
high-grade,  extensive  arterio-sclerosis,  there  was  observed 
during  her  lifetime  a  retention  of  urine  ("second  stage," 
according  to  Guyon)  ;  at  the  autopsy  320  c.c.  of  urine 
were  found  in  the  bladder,  and  the  proportion  of  the  com- 
ponents of  the  posterior  bladder  wall  was  from  i  :i.i8  to 
1:1.43.  In  case  47,  a  man  suffering  from  retention  of 
urine,  the  proportion  of  the  bladder  wall  components  was 
only  1:1.2.  (Contents  of  bladder  360  c.c).  The  last 
two  correspond  exactly  to  the  idea  of  Guyon's  "Pros- 
tatisme  vesical."  They  are,  therefore,  especially  impor- 
tant, because  in  neither  of  the  two  was  the  clinical  picture 
obscured  by  chronic  inflammatory  complications,  which 
deprive  the  only  corresponding  case  of  Bohdanowicz  of 
its  importance. 

The  first  of  my  two  observations  (case  44)  is  very 
similar  in  all  respects  to  the  universally  cited  observa- 
tion of  Chevalier  (17),  which  it  would  be  very  easy  to 
regard  wrongly  as  a  striking  proof  of  the  causative  re- 
lationship of  arterio-sclerosis  to  bladder  insufficiency. 
The  second  of  my  two  observations  (case  47)  stands  in 
a  strong  contrast  to  the  first;  because  there  was  no 


(1)  To  Chief  Physician  Prof.  Dr.  Parenski  and  to  Dr.  Pasz- 
kowslci,  who  have  supplied  me  with  all  the  necessary  histories, 
I  express  my  sincere  thanks. 


5° 


sign  of  arterial  sclerosis  to  be  discovered  in  the  or- 
ganism, and  still  the  proportion  of  the  bladder  wall  com- 
ponents corresponded  to  a  high-grade  pathological 
change.  But  the  cases  are  appropriate  for  comparison 
with  one  another,  because  in  the  second  case  (case  47) 
there  was  neither  a  prostatic  enlargement  nor  any  ob- 
struction to  the  flow  of  urine. 

There  is  still  another  valuable  observation  at  my  dis- 
posal (case  5);  in  this  .case  there  was  incontinence  of 
urine  with  a  full  bladder  during  lifetime  ("overflowing 
of  the   bladder,"   corresponding  to   the   third   stage   of 
Guyon's     "Ischuria    paradoxa").      At    the     autopsy    I 
found  the  bladder  greatly  dilated  (it  contained  62og.  of 
urine);  while  the  proportion  of  the  bladder  wall  com- 
ponents was  only  1:1.7.     The  apparent  increase  of  the 
connective  tissue  of  the  bladder  wall  at  the  expense  of 
the  muscle   was   in  this  case  less   pronounced   than  in 
the  two  cases  previously  mentioned.     This  circumstance 
is,  however,  by  no  means  capable  of  lessening  the  im- 
portance of  the  observations  already  cited;  because,   at 
any  rate,  the  lencroachment  on  the  normal  function  of  the 
bladder  sphincters,  during  the  formation  of  the  so-called 
Ischuria  paradoxa,  plays  also  a  main  role.     The  efflcien- 
cy  of  the  bladder  sphincter  was  in  the  present  case  en- 
tirely nullified  by  a  tumor  growing  from  the  posterior 
lip  of  the  orificium  internum  urethra,  at  the  level  of  the 
orifice,  and  pressing  the  sphincter  muscle  apart. 

Both  the  previously  mentioned  cases  0)f  primary  bladder 
inisuiificiency  (Prostatisme  vesical)  could  without  further 
consideration  be  used  for  the  elucidation  of  the  patho- 
genesis of  this  condition,  if  it  were  not  that  they  differ 
absolutely  in  one  point. 

Both  cases  showed  the  sam.e  symptoms  during  life  and 
the  same  structural  changes  of  the  bladder  wall.  But  in 
the  first  case  (case  44).  we  find  in  addition  a  nearly  gen- 
eral arterial  sclerosis,  especially  attacking  the  smallest 
arterial  branches  ramified  in  the  bladder  wall.  In  the 
second  case  (case  47)  we  encountered  nowhere  any 
atheromatous  changes  in  the  arteries,  neither  in  the  ves- 
sels of  the  genito-urinary  apparatus,  nor  anywhere  else  in 
fhe  organism  ;  and  still  the  clinical  manifestations  and  the 
anatomical  changes,  as  far  as  the  bladder  was  concerned, 
were  just  as  pronounced  as  in  the  first  case,  and  perhaps 

51 


even  more  so.  The  antithesis  which  occurs  in  these  cases 
is  only  to  be  explained  when  it  is  possible,  through  the 
verifying  investigation  of  a  larger  number  of  cases,  to 
find  how  far  the  changes  in  the  structure  of  the  bladder 
wall  run  parallel  with  the  atheromatous  changes  in  the 
smallest  intro-parietal  arteries  of  the  bladder.  By  em- 
ploying the  methods  of  investigation  utilized  in  the  pres- 
ent work,  it  was  proven  that  the  maximum  and  mini- 
mum' relative  numerical  values  of  the  arterial  media,  on 
the  one  hand,  and  the  thickness  of  the  wall  on  the  other, 
were  nearly  equal  to  the  maximum  and  minimum  numer- 
ical values  respectively  of  the  bladder  muscle.  At  least,  I 
found  this  to  be  the  fact  in  the  cases  investigated  by  my- 
self. 

I  ihave  already  mentioned  that  the  maximum  of  the 
proportion  between  the  connective  tissue  framework  and 
the  bladder  muscle  is  1:1.2;  the  minimum,  On  the  other 
hand,  is  1 14. 

The  proportion  of  the  intima  thickness  to  that  of  the 
media  ranges  between  the  following  limits :  Maximum 
about  1:1,  minimum  (ca)  1:5. 

The  proportion  of  the  lumen  diameter  to  the  thickness 
of  the  walls  oif  the  vessels  is  expressed  by  different  num- 
bers, but  its  quotient  is  alike  the  maximum  and  minimum 
respectively  of  the  other  two  numerical  proportions. 
In  general  this  quotient  amounts  in  all  these  three  nu- 
merical proportions  to,  maximum  average  i,  minimum 
average  0.25.  This  can  be  expressed  in  other  words,  as 
follows :  The  amount  of  connective  tissue,  in  the  highest 
degree  of  changes  in  the  structure  of  the  bladder  wall,  is 
the  same  as  the  amount  of  muscle.  In  the  highest  degree 
of  atheromatous  vessel  changes  (in  my  cases)  the  thick- 
ness oif  the  intima  and  media  is  the  same,  and  the  lumen, 
equals  the  wall  thickness.  In  minimum  changes  (which 
comes  near  to  the  normal  condition)  the  amount  of  the 
connective  tissue,  the  thickness  of  the  intima,  or  the  thick- 
ness of  the  wall  of  the  vessels,  respectively,  amounts-  to 
one-quarter  of  the  amount  of  the  muscle,  the  width  of  the 
media  or  the  lumen  of  the  corresponding  artery,  respect- 
ively. 

This  rule  refers,  of  course,  especially  in  its  second  part, 
only  to  the  intra-parietal  bladder  arteries,  and  ariiong 
these  especially  to  the  ones  which  have  an  equal  caliber. 

52 


It  does  not  seem  practicable  to  enumerate  here  the  simall 
synoptical  row  of  figures  which  contain  the  results  of  the 
micrometric  measurements.  I  think  it  wiser  to  recapitu- 
late the  results  of  my  investigation'  in  graphic  tables. 
(See  Tables  III.  and  IV.,  page  174.)  If  the  statement 
of  Launois,  that  "que  plus  les  vaisseaux  sont  modifies, 
plus  la  degemerescence  de  I'appareil  urinaire  est  accen- 
tuee,"  were  correct,  then  the  curve,  which  indicates  the 
increase  of  the  changes  of  the  structures  of  the  bladder 
wall,  must  run  nearly  parallel  to  that  which  represents 
the  increase  in  the  intensity  of  the  atheromatosis  of  the 
vessels.  The  courses  of  these  two  curves  are  essentially 
dififerent  in  the  accompanying  tables. 

In  Table  I II.,  the  intensity  of  the  atheromatous  changes 
in  the  vessels  is  expressed  by  the  relative  increase  of  the 
thickness  of  the  wall  of  the  vessel  (the  lumen  of  the  vessel 
is  taken,  as  the  unit).  I  rely  here  upon  the  fact,  almost 
universally  accepted,  that  the  lumen  of  the  small  arteries 
gets  continually  narrower  with  the  increase  of  the  in- 
tensity of  the  atherematous  changes  following  a  progres- 
sive thickening  of  the  vessel  wall. 

The  relative  numerical  values  of  the  wall  thickness  of 
the  arteries  are  arranged  in  arithmetical  order  in  Table 
III.  According  to  it,  the  connecting  curve  declines  uni- 
formly with  the  increasing  intensity  of  the  atheromatosis. 
The  relative  numerical  value  of  the  normal  arterial  wall 
stands  at  the  beginning  of  the  curve.  One  sees  that  in 
the  normal  intra-parietal  arteries  of  the  bladder  the 
lumen  amounts  to  three  times  as  much  as  the  thickness 
of  the  wall ;  the  arteries  which  are  changed  the  most  and 
in  which  the  thickness  of  the  wall  equals  the  diameter  of 
the  lumen  are  grouped  at  the  end  of  the  curve. 

The  relative  numerical  value  of  the  blad'der  muscle 
stands  in  the  same  vertical  column  in  which  the  numeri- 
cal value  of  the  arterial  walls  of  the  same  case  is  recorded. 
The  curve  representing  the  muscle,  and  which  at  the 
same  time  shows  the  change  in  the  relation  of  the  bladder 
wall  components,  runs  by  no  means  parallel  with  the 
arterial  curve;  it  is  represented  by  a  quite  irregular, 
broken  line.  The  contrast  in  the  behavior  of  the  two 
curves  is  very  striking.  Even  if  we  reconsider  the  in- 
dividual fluctuations  in  the  relation  of  the  components 
of  the  bladder  wall,  it  still  remains  impossible  to  discover 

53 


a  connection  of  this  change  with  the  behavior  of  the 
vessels.  On  the  left  side  of  the  table,  for  instance,  where 
the  arteries  are  nearly  unchanged,  we  find,  among  others, 
cases  also  in  which  the  changes  m  the  structure  of  the 
bladder  wall  were  most  strikingly  pronounced  (case  19, 
47).  On  the  right  of  the  table,  which,  on  the  other  hand, 
expresses  the  high-grade,  atheromatously  changed  ar- 
teries, we  encounter  among  others  the  highest  numerical 
values  of  the  bladder  muscle  which  I  have  had  the  oppor- 
tunity to  demonstrate  (case  51,  56). 

Table  IV  was  made  up  in  a  similar  way ;  only  here  the 
intensity  of  the  atheromatous  changes  in  the  arteries  was 
measured  on  a  basis  of  the  basis  of  the  relationship  of 
the  thickness  of  the  intima  and  media. 

We  also  observe  in  table  IV  that  the  uniformly  de- 
scending curve  of  the  arterio-sclerotic  changes  in  no  way 
expresses  the  course  of  the  line  representing  the  bladder 
muscle;  this  line  is  very  irregular,  now  ascending,  now 
descending. 

A  difference  between  these  two  tables  is  to  be  noted 
in  only  one  respect,  namely,  one  sees  that  in  table  IV 
the  higher  numerical  values  of  the  muscle  are  mainly 
(although  not  exclusively)  at  the  beginning  of  the  table; 
that  is,  in  the  vicinity  of  the  normal  behavior  of  the 
vessels.  The  cases  in  question  refer  tO'  young,  and  to  a 
certain  extent  normal,  individuals,  without  any  prostate 
enlargement.  The  final  result  of  our  micrometric  meas- 
urements seems,  therefore,  to  speak  against  the  most  im- 
portant, and,  at  the  same  time,  last  support  of  Guyon's 
theory.  The  statement  that  bladder  insufficiency  in  old 
people  stands  in  intimate  and  exclusive  relationship  to 
arterial  sclerosis  is  without  any  foundation. 

Although  I  also,  by  other  means,  came  to  the  same 
conclusion  with  regard  to  Guyon's  theory,  as  Caspar  and 
Bohdanowicz,  I  do  not  at  all  agree  in  the  other  state- 
ments made  by  these  two  investigators. 

On  the  basis  of  my  investigations,  I  believe  I  can 
maintain  that  senile  bladder  insufficiency  has  a  well- 
demonstrable  anatomical  foundation  in  the  form  of 
structural  changes  in  the  bladder  wall,  which  circum- 
stance was  put  down  by  Caspar  as  being  open  to  criti- 
cism. These  structural  changes  c-'nnot  be  brought  into 
a  causative  relationship  to  the  bladder  hypertrophy,  con- 

54 


trary  to  the  view  of  Bohdanowicz. 

In  one-half  of  my  observations  of  aged  male  individ- 
uals, and  in  all  my  cases  ol  aged  female  individuals,  I 
could  discover  no  trace  of  bladder  hypertrophy,  nor  a 
cause  for  it.  Later  on  this  will  be  considered  more  in 
detail.  And  still,  a  change  in  the  relationship  of  the  com- 
ponents of  the  bladder  wall  was  demonstrable  in  the 
majority  of  cases,  sometimes  of  a  high  degree,  and  in 
some  instances  it  was  even  the  cause  of  disturbances  of 
micturition  during  life  time. 

As  the  result  then  of  my  investigations  as  set  forth  in 
the  preceding  chapters  I  came  to  the  following  conclu- 
sions : 

First,  the  changes  of  the  prostate  gland  of  the  urinary 
bladder  and  of  the  kidneys  are,  in  the  cases  of  so-called 
"prostatismus,"  neither  synchronous  nor  co-ordinated, 
and  stand  in  no  relation  to  arterio-sclerosis;  neither  are 
they  if  one,  two  or  all  of  the  changes  of  the  organ  be 
present  in  the  same  individual,  concurrent  with  arterio- 
sclerosis. 

Second,  the  anatomical  basis  for  the  bladder  insuffi- 
ciency which  occurs  concurrently  with  so-called  "prostate 
hypertrophy,"  is  to  be  sought  in  a  quantitative  change  of 
the  component  parts  of  the  bladder  at  the  expense  of  the 
muscle  tissue.  The  latter  change  does  not  stand  in  a 
causative  relationship,  either  with  the  arterio-sclerosis  of 
the  small  intra-parietal  arterial  branches  of  the  bladder,  or 
with  the  hypertrophy  of  the  bladder  muscle. 


55 


CHAPTER    VI. 

CAUSES  OF  THE  ANATOMICAL  CHANGES  IN  THE 
WALL  OF  THE  URINARY  BLADDER 

The  guide  to  find  one  of  the  most  important  causes  of 
the  changes  in  the  structure  of  the  bladder  wall  is  given 
us  by  the  fact,  made  clear  by  Table  IV,  that,  in  young 
male  individuals  with  normal  genito-urinary  apparatus 
and  normal  vascular  system,  the  bladder  wall  is 
constantly  very  rich  in  muscular  elements.  Furthermore 
it  is  proven  that  the  thickness  of  the  intima  gives  us  a 
much  more  reliable  measure  of  the  normal  condition  of 
the  arteries  than  does  the  proportion  of  the  lumen  diam- 
eter to  the  thickness  of  the  wall.  The  cause  of  this  is 
probablv  that  the  adventitia,  which  ranges  inside  very 
broad  limits,  was  always  added  to  the  thickness  of  the 
wall. 

That  the  proportion  might  be  looked  over  more  clearly, 
I  arranged  all  my  cases  according  to  age.  From  the  ac- 
companying table  (Table  V),  which  shows  this  compila- 
tion in  the  form  of  a  curve,  one  can  see  that,  leaving  indi- 
vidual fluctuations  aside,  the  quantitative  changes  in  the 
hladder-ivaU  components  run  parallel  with  the  increase  in 
age,  and  become  more  pronounced  with  the  increase  in 
age,  this  is  especially  so  above  the  sixtieth  year. 

The  influence  of  age  is  made  still  more  evident  by  the 
second  curve,  in  which  the  average  values  of  the  different 
periods  of  age  are  grouped  together.  It  is  clearly  shown 
by  these  average  numbers  that  the  muscle  tissue  occupies 
about  i  of  the  bladder  wall  in  young  individuals,  while  in 
very  old  people  it  makes  up  hardly  2-^^  and  sometimes 
even  only  |. 

From  this  fact  we  must  conclude  that  the  quantitative 
changes  in  the  components  of  the  bladder  zvall,  in  which 

'  56 


the  anatomical  basis  for  bladder  insufificiency  is  to  be 
soug-ht,  is  produced  by  the  influence  of  age  and  develops 
in  the  majority  of  cases  parallel  with  the  increase  of  age. 
This  rule  is  of  course  by  no^  means  without  exception.  In 
a  fraction  of  the  number  of  cases,  even  in  cases  of  very 
old  individuals  (cases  8  and  41),  the  structure  of  the 
bladder  wall  is  only  insignificantly  changed :  above  the 
limits  formed  by  the  fiftieth  to  the  sixtieth  year  of  life 
the  muscle  tissue  does  not  exceed  the  connective-tissue 
framework  as  much  as  it  has  been  observed  to  exceed  this 
in  many  young  individuals  in  whom  the  muscle  tissue 
sometimes  makes  up  4-5  of  the  bladder  wall.  On  the  other 
hand,  we  meet  sometimes  with  a  very  marked  decrease 
in  the  musculatures  of  the  bladder  in  young  individuals, 
where  it  exceptionally  makes  up  only  2-3  of  the  bladder 
wall.  But  it  is  easy  to  verify  the  fact  that  this  lower 
limit  is  never  exceeded  before  the  fiftieth  year  of  life. 
The  border-line  is  formed  by  the  ten-year  period  between 
the  fiftieth  and  sixtieth  year.  In  this  period  are  to  be 
found  the  highest  as  well  as  the  lowest  numerical  values 
of  the  bladder  muscle :  the  connecting  line  of  this  period 
with  its  marked  curve  points  to-  the  fact  that  this  ten- 
year  period  is  a  critical  one  for  the  bladder. 

If  we  overlook  the  fluctuations  which  occur  within  the 
normal  limits,  we  shall  find  that  the  changes  in  the  struc- 
ture of  the  bladder  wall,  also  in  old  people,  are  by  no 
means  always  marked.  The  diminution  in  the  physiolog- 
ical function  of  the  organism  does  not  necessarily  coincide 
with  the  number  of  years  which  mark  the  beginning  of  the 
senile  state;  and,  just  as  the  senile  atrophy  of  some  inter- 
nal organs  is  by  no  means  a  constant  occurrence  in  old 
age,  just  as  little  do  the  changes  in  the  structure  of  the 
bladcler  wall,  which  must  be  attributed  to  the  senile  retro- 
grade occurrences,  coincide  with  a  certain  age.  For  this 
reason  these  changes  are  also  more  pronounced  in  individ- 
uals who  are  weak,  badly  nourished,  or  for  any  other 
reasons  are  emaciated,  than  in  others  of  the  same  age 
but  strongly  built  and  well  nourished.  Similarly  to  other 
organs,  changes  in  the  bladder  wall  may  appear  earlier  in 
these  emaciated  individuals  and  may  even  in  early  youth 
reach  an  exceptionally  high  grade,  and  may  even  cause 
disturbances  during  lifetime.  An  example  of  such  an 
early  atrophy  of  a  single  organ  is  often  met  with  in  the 

57 


dissecting'  room  in  the  form  of  an  early  muscle  atrophy 
of  the  heart,  as  is  daily  observed  in  emaciated  individuals. 
In  a  similar  way  such  an  early  atrophy  of  the  bladder 
muscle  may  also  occur,  producing  a  "spontaneous"  bladder 
insufficiency,  the  so-called  "prostatisme  vesical." 

We  cannot  discard  the  hypothesis  that  such  conditions 
occur  more  easily  and  sooner  in  individuals  who  are  born 
with  a  bladder  wall  poor  in  muscle  tissue.  The  early 
changes  in  the  structure  of  the  bladder  wall  may  of  course 
occur  without  any  senile  atrophy  in  another  organ,  just 
as  the  senile  or  the  early  atrophies  of  the  heart  or  the  kid- 
neys occur  individually.  As  an  example  of  such  an  early 
atrophy,  case  47  may  be  cited,  in  which  it  occurred  in  a 
56-year-old  man.  Now  the  important  question  presents 
itself  to  us,  what  changes  occur  in  the  bladder  wall  if  the 
prostate  suffers  a  pathological  change  ?  In  what  way  is 
bladder  insufficiency  produced  in  such  cases? 

It  cannot  be  denied  that  bladder  insufficiency  occurs 
often  in  old  people  attacked  by  a  so-called  "prostate  hy- 
pertrophy." The  "spontaneous"  bladder  insufficiency,  on 
the  other  hand,  is  a  rare  exception.  In  consideration  of 
this  circumstance  it  seems  "a  priori"  very  probable  that 
there  must  still  he  other  causes  for  the  disurbances  of 
micturition  in  cases  of  enlargement  of  the  prostate  gland. 
This  question  becomes  complicated  by  the  fact  that  the 
enlargement  of  the  prostate  gland  as  a  rule  produces  a 
working  (compensating?)  hypertrophv  of  the  bladder;  it 
is  also  to  be  decided  in  what  relation  bladder  hypertrophy 
stands  to  bladder  insufficiency. 

Still  further  the  question,  why  in  some  cases  of  en- 
largement of  the  prostate  there  occurs  no  disturbance 
of  micturition,  must  also  be  elucidated ;  because  precisely 
these  cases  were  brought  up  by  the  Parisian  school  as  a 
proof  that  prostate  hvpertrophy  is  not  to  be  regarded  as 
a  primary  cause  in  the  clinical  picture  of  the  so-called 
"prostatismus." 

I  shall  first  give  closer  attention  to  the  compensating  hy- 
pertrophy of  the  bladder  caused  by  the  enlargement  of 
the  prostate,  because  hy  this  I  hope  soonest  to  find  a  start- 
ing-point for  the  solution  of  other  not  less  important  ques- 
tions. 

An  enlargement  of  the  orostate  was  observed  in  one  half 
of  the  cases   (21)   of  old  men  which  I  examined.     The 

5S 


degree  of  this  enlargement  was  different  in  the  different 
parts  of  the  prostate,  and  therefore  the  form  of  the  pros- 
tate on  the  one  hand  and  of  the  orificium  vesicale  and  the 
pars  prO'Statica  urethra  on  the  other  showed  various  de- 
viations. To  save  space,  I  shall  not  enumerate  in  detail 
all  these  changes,  as  they  are  concisely  recorded  in  the  ac- 
companying table 


TABLE   VI. 
The  frequency  of  hypertrophy  of  the  bladder    wall. 
ion  to  the  emptying  of  the  bladder. 


Its  relation  to  the  obstruct-»; 


^ 

/I  thiroma 
0/  the  priMciph 

ll 

Weight 

Observed  condition   0/  the  Prostite  respecting 

|| 

II 

p; 

tranches  0/  the 

5  « 

0/  the 

th£  manner  0/  the  obstruction  disturbing 

^i 

g.^ 

■^  h 

1 

btadtUr  arteries. 

11 

frostate 

the  'outjiow  0/  Urine. 

|i 

■%4 

^ 

£1 

li 

:; 

^ 

1 

J 

31.2 

Turn  Excresc  on  side;  muse.  valve;dev.  led 

580 

, 

», 

3 

4 

Calcination 

25.J 

Dev.  toward  posterior  in  the  pars  prosl.  ureth. 

760 

4 

' 

«[> 

Slight  degree 

1 

33.5 

High  grade  deviation  toward  the  left 

160 

6 

I 

•1 

1 

Bladder-neck  valve 

620 

3 

I 

6 

Atheroma 

1 

247 

340 

5 

••l 

7 
8 
9 

• 

' 

34.0 

•5-3 

"               "        Int.  orifice  elevated. 

420 

450 
590 

5 

T 

I 

21.2 

540 

4.5 

IJ 

26.6 

.5.6 

Deviation  toward  the  right;  blad.  neck  valve 

310 

6 
5 

"%> 

>3 

, 

26.0 

on  right;  muac.        "        "        " 

280 

3.5 

t 

4 

1 

'4 

Wall   thickened 

t 

39.0 

Bladder-neck  valve 

780 

3 

Calcination 

30.8 

290 

8 

); 

i6 

36.2 

*'                " 

430 

6 

« 

■7 

'* 

23.7 

Deviation  on  right;  bladder-neck  valve 

400 

7 

^ 

i8 

30.0 

300 

3 

< 

!l 

1 

11 

27.3 

toward  the  right 

280 

7 

42. 5 

"        posterior;  high  gr.  deformity 
left;  bladder-neck  valve 

700 

8 

59 

44 -o 

900? 

5 

7 

"i" 

■  8 

16 

5 

.3 

1 

~ 

Atheroma 

_ 

12.0 

320 

3 

.i 

21 

Wall  thickened 

■  2.5 

9 

•^ 

24 

1 

■7.5 

210 

5 

=3 

14.0 

190 

4-5 

24 

Mod.  thickened 

t 

17.0 

5-5 

4? 

25 
26 
2? 

■3-3 
13.2 

80 

8 
6 

5 

I 

4 

28 

'9 

Calcination 

1 

18^3 
'5.4 

190 
60 

5-5 
6 

■j 

30 

12.4 

100 

5 

•^ 

31 

.9.0 

500 

3 

"!' 

32 

33 

Atheroma 

12.6 

260 

8 
5 

1 

34 

I 

■9-4 

300 

3 

11 

"5-5 

■  4.6 

310 

8 
3 

37 

■  2.8 

5-5 

■^ 

38 

1 

14.2 

300 

,4 

1 

39 

Wall  thickened 

16.8 

130 

S.5 

40 

Calcination 

■ 

19. 1 

5 

4" 

Slight  degree 

I 

250 

4 

1 

42 

1 

140 

5 

1 

43 

Wall  thickened 

1 

100 

5 

^ 

44 

1 

320 

3-5 

JtL. 

Calcination 

44° 

2-5 

i 

46 

47 

18.0 
•7.5 

(Average  Volume  of  the  Bladder  in   an    Adult 

300 
360 

3 

\l 

12.6 

200-400  ccm.    Thickness  of  the  contracted 

6 

1 

49 

8.3 

wall  of  the  bladder   12mm.    Thickness  of 

260 

4 

i 

50 

11.9 
15,5 

the  Bladder  wall  when  moderately  fill- 

80 

7 
6 

t 

52 

<5.o 

ed  3—4  tnm  (inclusive  of  submucous 

5 

T 

53 

■7-3 
7-7 
■  T'.o 

and  the  subserous). 

60 

' 

1 

54 

55 

(ViEBORDT,  Anal.  Datcn) 

150 

*■} 

jL 

■9-5 

8 

.^ 

58 

'9 

IT 

16 

42 

<» 

59 


In  general  I  demonstrated  such  anatomical  changes  in 
the  orifiicium  vesicale  and  in  the  pars  prostatica  urethra 
in  i8  of  the  21  cases  of  prostate  enlargement;  and  these 
changes,  either  only  one  of  them  or  all  combined,  were 
capable  of  producing  a  disturbance  in  the  free  outflow  of 
urine.  In  the  three  remaining  cases  (cases  3,  13  and  18) 
such  changes  were  not  to  be  found. 

The  question  whether  these  changes  could  really  pro- 
duce an  obstruction  to  the  free  outflow  of  urine  can  find 
its  solution  only  in  the  behavior  of  the  bladder.  Bladder 
hypertrophy  was  present  in  16  of  the  18  cases;  it 
was  missing  in  two  cases,  although  in  these  two 
cases  there  were  well-marked  changes  in  the  ori- 
ficium  vesicale  and  in  the  pars  prostatic  urethra.  In 
one  of  these  cases  (case  4)  the  prostate  gland  was  greatly 
enlarged  (weight  33.5  grms).  As  this  enlargement  oc- 
curred mainly  in  the  right  lobe  the  course  of  the  prostatic 
urethra  showed  a  marked  angular,  left-sided,  pathological 
deviation. 

The  frequency  of  hypertrophy  of  the  bladder  zvall.  Its 
relation  to  the  obstruction  to  the  emptying  of  the  bladder. 

In  the  other  case  (case  5)  the  prostate  weighed  only 
20.2  grms. ;  but  a  polypoid  tumor,  of  the  size  of  a  hazel- 
nut, extended  from  the  orificium  internum,  and  seemed 
to  have  its  origin  in  the  posterior  lip  of  the  orifice.  As 
this  tumor  was  pedienculated  and  freely  movable,  there  is 
no  doubt  that  it  was  capable  of  acting  as  a  valve  during 
the  contractions  of  the  bladder  and  of  shutting  off  the 
outflow  of  the  collected  urine  during  the  contractions  of 
the  bladder.  Why  a  compensating  hypertrophy  of  the 
bladder  muscle  was  not  developed  in  both  these  cases  is 
easily  answered.  Both  cases  were  very  old  and  very 
emaciated  men  (one  was  67,  the  other  yy  years  old).  In 
one  of  the  cases  there  was  present  a  marked  anaemia,  due 
to  hemorrhages  from  an  ulcus  rotundum  ventriculi,  while 
in  the  other  extensive  tubercular  changes  were  present; 
in  both  cases  I  found  senile  atrophy  of  the  internal  or- 
gans. The  organism  in  both  cases  was  under  the  poor- 
est conditions  of  life  and  its  vital  powers  had  greatly  suf- 
fered during  a  long  period  of  diminution.  From  this  it 
is  apparent  that  hypertrophy  of  the  bladder  musculature 
could  no  longer  occur.  Correspondingly  there  occurred 
also  in  the  second  of  the  cases  cited,  the  older  and  more 


60 


debilitated  individual,  during  lifetime  an  involuntary- 
Voiding  of  urine  by  reason  of  an  overdistended  bladder 
("Ischuria  paradoxa"). 

I  think  that  I  must  here  cite  the  axiom  which  served  as 
my  guide  in  the  decision  of  the  question  whether  the 
bladder  wall  was  hypertrophic  or  not.  I  have  already 
mentioned  that  from  the  results  of  the  micrometric  meas- 
urements executed  by  myself  neither  positive  nor  nega- 
tive conclusions  can  be  drawn  in  regard  to  an  increase  in 
the  bladder  muscle.  That  this  increase  really  occurs  can 
only  indirectly  be  inferred  from  the  thickness  of  the  wall. 
I  take  it  as  a  well-known  and  indisputable  fact  that  as  the 
bladder  becomes  stretched  it  becomes  to  a  certain  extent 
thinner.  Viervordt  states  (Anat.  Daten  und  Tabellen) 
that  the  entire  bladder  wall,  i.  e.,  the  muscle  with  its  con- 
nective-tissue framework,  the  mucous  membrane,  the 
submucosa  and  subserosa,  measures  in  the  adult  on  an 
average,  with  a  moderately  filled  bladder  (200-400  c.c), 
3-4  m.m  in  thickness ;  in  a  completely  contracted  bladder 
the  wall  thickness  reaches  almost  12  m.m.  By  numerous 
measurements  of  the  muscle  with  its  connective-tissue 
framework  (with  hand  lens)  in  young  individuals  in 
whom  there  was  no  pathological  deviation  in  the  genito 
urinary  system,  I  obtained  the  following  values  of  the 
thickness  of  the  bladder  wall  (compare  also  Table  VI). 
In  a  completely  contracted  bladder,,  y-d>  m.m 
Containing  60-80  c.c.  of  urine,  about  6  m.m 
"  100-150  c.c.         *'  ''         4-5  m.m. 

"  260  c.c.         "  "  4  m.m. 

"  300-360  c.c.         "  "  3  m.m. 

If  in  consequence  of  an  obstruction  to  the  free  out- 
flow of  urine  a  compensating  hypertrophy  is  formed,  then 
the  bladder  wall  must,  of  course,  increase  in  thickness. 
If  the  connective-tissue  framework  of  the  bladder  wall 
has  not  by  this  suffered  an  increase,  then  the  relative  value 
of  the  bladder  muscle  must^  of  course,  be  correspond- 
ingly larger.     (N.  B.  in  uncomplicated  cases.) 

It  is  easy  to  convince  oneself  of  the  correctness  of  this 
supposition  by  appropriate  examples. 

In  case  11,  for  instance,  the  bladder  contained  310  c.c. 
of  urine.  The  bladder  wall  was  6  m.m  thick.  The  pro- 
portion of  the  amount  of  the  connective-tissue  frame- 
work to  that  of  the  muscle  was  i  :3.i4. 

61 


Normally  the  bladder  wall  measures,  with  a  correspond- 
ing amount  (300-360  c.c.J  onh'  2-3  m.m  in  thickness. 
The  proportion  here,  as  previously  mentioned,  averages 
1 :2.8,  at  the  most  i  :3.  In  this  case  there  was  thus 
formed,  as  proved  by  measurements,  an  indisputable  blad- 
der h3'-pertrophy,  due  to  an  obstruction  to  the  free  out- 
flow of  urine. 

Likewise  in  case  14.  In  a  well-nourished,  and  by  no 
means  old,  indiviaual  there  was  a  marked  obstruction  to 
the  outflow  of  urine ;  the  bladder  extremely  dilated  and 
overfilled  with  urine,  with  contents  of  780  c.c.  The 
thickness  of  the  bladder  wall  was  3  m.m.  The  proportion 
of  the  components  of  the  bladder  wall  was  i  :3.  From 
the  quoted  empirical  scale  it  may  be  on  the  other  hand 
seen  that  when  the  bladder  contains  360  c.c.  the  bladder 
wall  measures  less  than  2-3  m.m.  in  thickness.  From  this 
one  would  assume  that,  presupposing  the  possibility  of 
such  a  phenomenon,  the  normal  bladder  wall,  in  a  bladder 
containing  800  c.c.  would  be  as  thin  as  paper.  In  our 
case  it  is,  on  the  contrary,  fully  3  m.m.  thick,  therefore 
indisputably  hypertrophic.  This  thickening  is  without 
doubt  to  be  referred  to  an  increase  in  the  muscle  tissue 
itself,  because  the  proportion  of  the  components  of  the 
bladder  wall  in  our  case  amounts  to  just  as  much  as  in  the 
bladders  of  healthy  and  young  individuals ;  considering 
the  advanced  age  of  the  individual,  the  preponderance  of 
the  connective-tissue  was  rather  to  be  expected. 

On  the  basis  of  other  similar  cases,  in  which  there  was 
no  inflammatory  complication  which  would  have  been 
capable  of  producing  a  thickening  of  the  bladder  wall 
without  hypertrophy  of  the  muscle  through  a  genuine, 
-active  proliferation  of  the  connective-tissue,  I  believe  I 
can  maintain  that  the  existence  or  the  absence  of  a  true 
hypertrophy  of  the  bladder  muscle  can  be  demonstrated 
with  some  correctness  by  my  method  of  investigation.  I 
presumed  before  this,  on  account  of  the  structure  of  the 
connective-tissue  framework  of  the  bladder  wall,  that  the 
connective-tissue  did  not  play  an  active  part  in  the 
changes  in  the  proportion  of  the  components  of  the  blad- 
der wall,  i.  e.,  it  was  not  hypertrophied.  Evidence  in  favor 
of  this  supposition  was  given  in  a  comparison  of  the  state 
of  normal  bladders  to  bladders  of  very  old  individuals  in 
which  there  was  neither  obstruction  to  the  outflow  of 

63 


urine  nor  hypertrophy  of  the  bladder.  In  cases  48  and 
30,  for  instance,  the  bladder  contents  was  in  each  100 
c.c. ;  in  the  first  the  bladder  wall  was  6  m.m.  thick,  in  the 
second  5  m.m.  The  proportion  of  the  components  of  the 
bladder  wall  in  the  first  was  i  :3,  in  the  second  i  :2.  If,  as 
I  assume,  in  the  change  in  the  proportion  of  components  of 
the  bladder  wall  the  atrophy  of  the  muscle  tissue,  and  not 
the  active  proliferation  and  increase  of  the  connective- 
tissue  framework,  plays  the  main  role,  then  the  bladder 
wall  in  the  uncomplicated  cases,  under  similar  conditions 
(an  equal  amount  of  urine),  must  sufi:er  a  thinning-out 
parallel  to  the  degree  of  this  change ;  at  any  rate,  it  can- 
not become  thicker. 

The  two  cases  cited  establish  this  presupposition  com- 
pletely. Far  be  it  from  me  to  maintain  that  the  changes 
in  the  structure  of  the  bladder  wall  that  have  been  con- 
sidered are  exclusively  formed  without  the  active  partici- 
pation of  the  connective-tissue  framework.  I  believe  only 
that  this  is  the  rule  for  the  uncompUcatcd  cases.  One 
must  not  forget  in  judging  these  conditions  that  in  every 
case  we  have  to  figure  with  individual  fluctuations;  that 
these  fluctuations  are  also  found  to  a  great  extent  in 
young  individuals,  and  their  existence  must  therefore 
also  be  taken  into  consideration  in  old  people. 

I  have  already  mentioned  that  the  connective-tissue 
framework  in  the  bladder  wall  becomes  denser  and  more 
compact  in  consequence  of  chronic  inflammatory  compli- 
cations. I  emphasize  here  that  this  manifestation  is  regu- 
larly to  be  observed  in  young  individuals  suffering  from 
chronic  inflammation  of  the  bladder  who  have  no  obstruc- 
tion to  the  outflow  of  urine.  In  these  cases  we  have  to 
deal  with  a  real,  absolute  increase  of  the  connective-tissue 
of  the  bladder  wall,  which  expresses  itself  in  the  relative 
preponderance  of  the  former  and  at  the  same  time  pro- 
duces a  marked  thickening  of  the  bladder  wall.  These 
conditions  allow  us  to  solve  directly -the  question  whether 
such  an  inflammatory  complication  alone,  without  the 
assistance  of  other  influences,  is  capable  of  producing  a 
change  in  the  proportion  of  the  components  of  the  bladder 
wall.  The  chronic  bladder  inflammations  are,  therefore, 
aside  from  the  influence  of  age,  of  the  greatest  impor- 
tance for  the  structure  of  the  bladder  wall. 

As  examples  of  this,  cases  19  and  47  may  be  not  quoted. 

63 


In  the  latter  case  inflammatory  complication  was  present, 
and  the  influence  of  old  age  was  responsible  for  the  occur- 
rence of  the  disturbance  of  the  equilibrium  of  the  com- 
ponents of  the  bladder  wall.  Entirely  different  is  case  19, 
in  which  the  relative  preponderance  of  the  connective- 
tissue  of  the  bladder  wall  reached  an  equal  degree.  Other 
factors  besides  the  influence  of  age  were  here  at  play — 
either  an  inflammatory  complication  or  an  obstruction  to 
the  outflow  of  urine.  Correspondingly,  the  bladder,  wall 
in  case  19  was  7  m.m.  thick  (instead  of  4  m.m.,  as  nor- 
mally), with  a  bladder  contents  of  280  c.c. ;  while  in  case 
47  the  thickness  of  the  bladder  wall  was  only  2  m.m. 
(instead  of  the  normal  3  m.m.)  In  both  cases  the  bladder 
musculature  itself  was  atrophic.  Consequently,  in  case 
47  the  bladder  wall  showed  a  thinning-out,  while  the 
connective-tissue  framework  remained  "in  statu  quo."  In 
case  19,  on  the  contrar}^  the  bladder  wall  was  very  much 
thickened,  due  mainly  to  an  active  increase  of  the  con- 
nective-tissue. These  two  cases  illustrate  clearly  what  an 
important  role  the  inflammatory  complications  play  in  the 
production  of  bladder  insufficiency.  The  intimate  con- 
nection of  this  inflammatory  complication  with  bladder 
insufficiency  is  proved,  however,  by  the  long-known,  un- 
yielding- sclerotic  bladders,  which  the  clinician,  as  well  as 
the  anatomist,  often  meets. 

The  foregoing  analyses  make  it  clear  to  us  why  in  some 
cases  even  with  a  very  extensive  prostate  enlargement 
there  is  no  bladder  insufficiency.  This  insufificiency  does 
not  happen  when  the  proportion  of  the  components  of  the 
bladder  wall  remains  within  the  normal  physiological 
limits,  or  else  when  it  oversteps  these  limits  exclusively  in 
favor  of  the  muscle.  In  the  latter  case  the  obstruction  to 
the  outflow  of  urine  is  entirely  compensated  for  by  the 
compensatory  hypertrophy  of  the  bladder  musculature. 
This  happens,  however,  very  seldom  in  the  diseases  which 
we  are  now  considering,  because  the  prostate  enlargement 
is  generally  found  in  old  people,  in  whom  the  capability 
for  an  active  hypertrophy  of  the  musculature  is  lost.  The 
other  possibility  seems  to-  be  much  more  frequent ;  that  is, 
the  proportion  of  the  components  of  the  bladder  wall  re- 
mains within  the  normal  limits,  or  there  is  a  very  insig- 
nificant disturbance,  which  is  not  capable  of  influencing 
the  functional  ability  of  the  bladder.     However,  this  is 

64 


possible  only  under  two  conditions,  namely,  when  the  hy- 
pertrophy of  the  prostate  causes  only  a  very  small  ob- 
struction to  the  outflow  of  urine,  as,  for  instance,  in  some 
cases  of  symmetrical  and  regular  enlargement  of  both 
lobes;  or  when  the  damages  which  we  refer  directly  to 
the  influence  of  age  did  not  act  long  enough  to  affect  the 
function  of  the  bladder.  These  two  conditions  are  pres- 
ent in  cases  3,  13  and  18.  The  absence  of  hypertrophy 
of  the  bladder  and  the  behavior  of  the  enlarged  prostate 
prove  that  in  these  cases  no  obstruction  to  the  outflow  of 
urine  existed.  The  age  not  at  all  advanced ;  a  good  gen- 
eral condition  of  nutrition;  the  behavior  of  all  the  in- 
ternal organs ;  the  fact  that  in  none  of  these  cases  was 
there  to  be  observed  any  sign  of  senile  atrophy,  while  in 
all  three  death  was  caused  by  an  acute  disease — all  these 
circumstances  explain  the  behavior  of  the  bladder  wall, 
which  structure  Avas  only  insignificantly  altered. 

In  judging  the  complicated  cases  of  the  so-called  pro- 
statismus  it  was  necessary  to  decide  whether  the  presence 
of  an  obstruction  disturbing  the  outflow  of  urine  had  any, 
and  then  what,  significance  for  the  condition  of  the  blad- 
der wall,  and  that  at  a  time  when  the  bladder  muscle  had 
partially  or  entirely  lost  the  capability  of  becoming  hyper- 
trophied.  Furthermore,  we  had  to  judge  what  relation 
exists  between  the  influence  of  an  established  obstruction 
and  the  influence  of  age. 

For  this  purpose  I  separated  the  cases  in  which  there 
was  an  obstruction  to  the  outflow  of  urine  due  to  a  pros- 
tate enlargement  from  the  cases  without  any  disturbances. 

The  proportion  of  the  components  of  the  bladder  wall 
in  each  individual  case  was  represented  graphically,  simi- 
larly as  in  the  previous  Tables. 

It  will  be  seen  from  Table  VII  that  in  both  groups  the 
influence  of  age  is  very  pronounced.  In  both  groups  the 
average  numerical  value  of  the  bladder  musculature  is 
very  low  for  the  higher  ages ;  these  values  were  much 
smaller  with  established  obstructions  than  in  cases  in 
which  no  obstruction  could  be  demonstrated.  From  this 
we  may  conclude  that  the  average  numerical  value  of  the 
bladder  muscle,  measured  with  the  numerical  value  of 
the  connective-tissue  of  the  bladder  wall  as  a  unit,  is 
smaller  under  conditions  otherwise  similar  if,  besides  the 
influence  of  age,  changes  in  the  vicinity  of  the  orificium 

65 


and  the  prostatic  urethra  produce  their  injurious  efifects 
upon  the  bladder  wall.  P'rom  this  it  is  clear  that  bladder 
insufficiency  is  more  easily  and  more  frequently  formed 
in  old  people  with  prostate  enlargement  than  in  those  in 
whom  the  prostate  is  not  enlarged,  or  is  respectively 
smaller.  In  the  first  cases  this  is  to  be  referred  to  the 
higher  degree  of  the  changes  in  the  structure  of  the  blad- 
der wall. 

The  cause  of  the  more  frequent  appearance  of  bladder 
insufficiency  in  old  people  with  prostate  enlargement  is 
by  no  means  to  be  sought  exclusively  in  the  more  pro- 
nounced changes  in  the  bladder  wall.  Undeniably,  also, 
the  degree  of  the  obstruction  to  the  outflow  of  the  urine 
is  very  significant.  The  more  disturbing  the  operation  of 
such  an  obstruction  is  upon  the  outflow  of  urine,  the  less 
important  the  changes  in  the  structure  of  the  bladder  wall 
that  will  be  necessary  to  cause  symptoms  during  life- 
time. Vice  versa,  with  more  pronounced  changes  in  the 
bladder  wall  a  relatively  small  obstruction  is  capable  of 
nullifying  the  functional  equilibrium.  The  final  result  of 
all  the  injurious  factors  is  therefore  different  in  each  in- 
dividual case,  and  one  is  hardly  capable  of  determining  it 
beforehand  from  the  anatomical  conditions.  In  one  case, 
for  instance,  the  structure  of  the  bladder  wall  may  re- 
main nearly  unchanged,  and  the  cause  of  the  disturbance 
of  micturition  lies  here  exclusively  in  the  important  local 
obstruction  to  the  outflow  of  urine.  A  surgical  inter- 
ference which  removes  this  local  obstruction  is  in  this 
case  capable  of  restoring  the  function  of  the  bladder  with- 
out any  trouble.  Of  two  individuals  in  which  the  changes 
in  the  bladder  wall  reach  a  similar  degree,  one  in  whom 
there  exists  no  enlargement  of  the  prostate  will  not 
suiTer  from  any  disturbance  of  micturition,  while  the 
other  with  prostate  enlarged  will  show  pronounced  symp- 
toms of  retention.  In  a  fourth  case,  finally,  there  exists 
nO'  obstruction  disturbing  to  the  outflow  of  urine,  and  the 
disturbance  of  micturition  in  this  cas'e  has  its  origin  in  a 
high-grade  atrophy  of  the  bladder  muscle.  It  is  to  such 
cases  that  the  name  "prostatisme  vesical"  is  given.  This, 
in  part  at  least,  answers  the  question  why  the  function  of 
the  bladder  is  restored  in  a  few  cases  only  after  castration. 
Provided  that  the  prostate  atrophies  in  some  c^ses  after 
castration,  then  the  proposition  that  sometimes  just  those 

66 


parts  of  the  prostate  become  smaller  which  formed  the 
main  ohstrnction  to  the  outflow  of  urine  is  not  to  be  cast 
aside.  The  final  result  of  a  castration  with  regard  to  the 
.  function  of  the  bladder  depends  only  on  the  momentary 
condition  of  the  bladder  wall  in  such  cases.  If  the  struc- 
ture of  the  bladder  wall  be  relatively  little  changed,  then 
the  function  of  the  bladder — though  obscured  to  a  certain 
extent  by  the  local  obstruction,  but  otherwise  only  little 
attacked — will  be  entirely  restored;  in  another  case  the 
result  of  a  surgical  interference  will  be  unsatisfactory, 
and  the  condition  of  the  patient  is  slightly  or  else  not  at 
all  changed. 

In  this  respect  there  is  no  essential  difi^erence  between 
the  castration  and  the  interferences  which  aim  at  a  direct 
removal  of  the  obstruction  to  the  outflow  of  urine,  that  is, 
operations  executed  on  the  prostate  itself.  The  restora- 
tion of  the  function  of  the  bladder  after  castration  is 
therefore  not  a  mystery,  and  it  is  also  entirely  unnecessary 
to  search  for  other  forced  explanations. 

My  investigations  show  satisfactorily  that  the  term 
"prostatismus,"  convenient  as  it  may  be,  does  not  corre- 
spond to  a  uniform  clinical  and  anatomical  picture.  It 
gives  no  basis  for  a  uniform  anatomical  change  composed 
of  co-ordinated  symptoms  produced  by  a  conditio-nal^ 
single,  general  cause.  The  sym.ptoms  of  bladder  insuffi- 
ciency, as  occurring  in  some  old  people,  are  more  related 
to  anatomical  changes  O'f  different  kinds,  and  are  to  be 
regarded  as  sequels  of  different  causes.  It  cannot  be  de- 
nied, in  cases  where  a  bladder  insufficiencv  occurs  con- 
currently with  a  prostate  enlargement,  that  the  latter  is  by 
no  means  tO'  be  regarded  as  insignificant. 

I  may  summ.arize  the  results  of  my  investigation  in  the 
following  sentences : 

(i)  The  clinical  symptoms  of  the  so-called  "prostatis- 
mus"  are  without  a  uniform  anatomical  basis,  no  matter 
whether  they  occur  in  old  men  suffering  from  hypertrophy 
of  the  prostate  gland,  or  in  individuals  in  whom  the  pros- 
tate is  of  normal  size  or  atrophic,  or  in  female  subjects. 
The  anatomical  changes  which  are  expressed  by  these 
clinical  symptoms  are  neither  co-ordinated  nor  uniform ; 
nor  are  they  produced  by  a  uniform  general  cause.  Espe- 
cially is  it  true  that  we  cannot  look  upon  arterio-sclerosis 
as  a  common  cause  for  the  changes  which  occur  in  the 

67 


kidneys,  the  bladder  and  the  prostate  during  the  course  of 
the  so-called  "prostatismus." 

(2)  One  of  the  anatomical  bases  of  bladder  insuffi- 
ciency is  to  be  sought  in  a  quantitative  change  in  the  pro- 
portion of  the  muscle  tissue  and  connective-tissue  of  the 
bladder.  This  change  seems  in  the  majority  of  cases  to 
have  its  cause  in  the  atrophy  of  the  muscles  of  the  blad- 
der. A  real,  active  increase  of  the  connective-tissue  of 
the  bladder  wall  seems  only  to  follow  frequently  occur- 
ring chronic  inflammation  of  the  bladder. 

In  the  cases  in  which  there  is  a  change  in  the  form  of 
the  orificium  vesicale  urethra  and  a  change  in  the  course 
of  the  prostatic  urethra  due  to  the  hypertrophy  of  the 
prostate  gland,  part  of  the  symptoms  may  be  directly 
ascribed  to  this  mechanical  interference.  After  remov- 
ing this  obstacle  the  function  of  the  bladder  may  be 
brought  to  normal,  provided  the  wall  of  the  bladder  suf- 
fered no  marked  changes  in  structure. 

(3)  The  changes  mentioned  in  the  structure  of  the 
bladder  wall  occur  more  frequently  with  the  increase  in 
age.  In  the  individuals  examined  by  myself  the  degree 
of  these  changes  was  parallel  with  the  age.  A  higher  de- 
gree of  these  changes  is  reached  in  those  cases  only  in 
which,  in  addition  to  the  influence  of  old  age,  there  is  an 
injurious  effect  of  mechanical  interference  with  the  out- 
flow of  urine,  and  in  which  at  the  same  time  the  muscle 
has  lost  its  capability  to  become  hypertrophic ;  but  the 
highest  degree  is  only  reached  when  to  these  injurious  in- 
fluences is  added  a  chronic,  inflammatory  process. 

In  the  majority  of  the  cases  of  bladder  insufficiency  in 
old  people  all  these  three  injurious  influences  occur  at  the 
same  time.  In  rarer  cases  two,  and  exceptionally  even 
one,  of  these  injurious  influences  may  produce  a  high  de- 
gree of  anatomical  and  clinical  disturbances.  In  cases  in 
which  there  is  an  ostacle  to  the  outflow  of  urine  due  to 
an  enlargement  of  the  prostate  gland,  this  may  be  partly 
or  wholly  compensated  for  by  the  compensating  hvper- 
trophy  of  the  bladder,  which  is  only  exceptionally  absent. 


68 


CHAPTER  VII. 

THE    CHANGES    IN    THE    ORIFICIUn     VESICALE 

URETHRAE  PRODUCED  BY  THE  EN= 

LARGEflENT    OF  THE  PRO= 

STATE   GLAND 

THE  ORIGIN  OF  THE  SO-CALLED  "SENILE  BLADDER  WEAKNESS. 

The  kind  of  the  obstruction  to  the  outflow  of  urine  de- 
pends upon  what  part  of  the  prostate  gland  is  the  most 
enlarged. 

In  an  insignificant  enlargement  which  uniformly  in- 
volves both  lateral  lobes  of  the  prostate,  and  which  does 
not  produce  a  special  prominence  of  the  so-called  "middle 
lobe,"  the  prostatic  urethra  may  be  only  slightly  changed, 
and  the  free  outflow  of  urine  may  not  be  interfered  with 
to  any  extent.  This  was  observed  in  three  of  my  cases 
(3,  13  and  18).  As  soon  as  one  part  of  the  prostate  is  en- 
larged more  than  the  others,  and  as  soon  as  the  "hyper- 
trophy" of  the  two  lateral  lobes  reaches  a  higher  degree, 
then  either  the  orificium  vesicale  or  the  pars  prostatica 
urethra,  or  both,  must  undergo  changes  in  form,  which 
are  not  without  effect  on  the  free  outflow  of  urine. 

Far  be  it  from  me  to  take  up  a  consideration  in  detail  of 
all  the  kinds  of  changes  to  which  the  urethra  is  exposed 
in  consequence  of  an  enlargement  of  the  prostate.  I 
would  then  have  to  go  over  things  which  have  been  thor- 
oughly investigated,  and  which  have  long  been  generally 
known. 

Pathological  anatomv  has  in  this  respect  brought  out 
all  that  was  to  be  l)rought  out,  and  the  excellent  investiga- 

69 


tions  of  Socin  (i  19),  Guyon  (40,  41,  44,  47  )  and  Thomp- 
son (130,  132,  133),  aside  from  their  predecessors  and 
successors,  will  always  form  the  basis  for  further  work 
in  diis  field. 

The  changes  in  the  orificium  vesicale  still  up  to  the 
present  time,  give  cause  for  divergent  views,  especially 
in  so  far  as  regards  the  meaning  of  certain  clinical  symp- 
toms. In  particular  it  was  argued  for  a  long  time  that  in 
anatomical  changes  of  the  orifice  the  cause  of  retention  of 
urine  (Ischuria)   is  to  be  sought. 

In  the  previous  chapters  I  tried  to  explain  how  great 
a  part  the^  structural  changes  in  the  bladder  well  play  in 
the  production  of  symptoms  of  the  so-called  prostatismus. 
I  came  to  the  conclusion  that  sometimes  the  bladder  wall 
may  remain  entirely  unchanged,  or  may  suffer  only  slight 
change.  The  cause  of  the  disturbance  in  micturiton  is, 
then,  to  be  sought  exclusively  in  the  local  changes  in  the 
orificium  and  the  pars  prostatica  urethrse.  I  am  willing 
to  assume,  then,  on  the  basis  of  my  own  observations  and 
of  numerous  casualties,  that  cases  in  which  the  disturb- 
ances of  micturition  are  entirely  and  only  due  to  changes 
in  the  orificium  internum,  "sensu  stricto,"  do  not  exist  at 
all  or  are  at  most  rarities.  This  view  is  verified  by  well- 
known  statistics.  Thompson,  in  his  comipilation  of  125 
cases  of  prostate  hypertrophy,  states  that  he  saw  only 
three  cases  of  isolated  changes  in  the  orificium  vesicale 
in  the  form  of  a  so-called  hypertrophy  of  the  middle  lobe. 
Motz  (89a),  who  collected  sixty  cases  in  all,  from  the 
literature,  found  only  four  similar  observations.  Also 
Sversen  (64),  who  examined  203  prostates,  noted  among 
fifty-two  hypertrophied  glands  only  four  in  which  the  en- 
largement attacked  exclusively  the  so-called  middle  lobe 
[1.  c.  p.  32(1)].  Among  my  own  observations  there  is 
really  not  a  single  one  in  which  the  changes  were  ex- 
clusively confined  to  the  orincium  without  attacking  at  the 
same  time  the  prostatic  urethra.  At  any  rate,  we  must 
maintain  firmly  the  position  that  Ischuria  has  its  cause  in 
different  kinds  of  changes  in  the  orificium  internum,  and 
that  different  mechanisms  play  a  role  here. 

Busck  (10)  constructed  from  the  investigation  which 
he  performed,  together  with  Koster  in  1877,  the  following 
mechanism.  The  orificium  vesicale  in  a  prostate  hyper- 
trophy projects  forward  against  the  lumen  of  the  bladder 

70 


in  the  form  of  an  obtuse  cone.  During  the  moment  of  a 
contraction  of  the  bladder  a  hydrostatic  pressure  against 
the  orificium  is  formed,  which  affects  the  whole  upper 
•surface  of  the  cone-shaped  projecting  orificium. 

By  these  means  the  lumen  of  the  urethra  is  compressed, 
and  an  emptying  of  the  bladder  becomes  impossible.  Op- 
posing Busch's  statements,  Jurie  (67)  replied  that  the 
anatomical  changes  of  the  orificium  vesicale  that  have 
been  describe  occur  relatively  seldom  in  proportion  to  the 
frequency  of  senile  (fisturbances  in  micturition.  On  the 
other  hand,  Jurie  lays  stress  upon  the  importance  of  other 
causative  movements  for  the  development  or  retention  of 
urine,  especially  the  weakening  of  the  muscle  fibres  of  the 
base  of  the  bladder  antagonistic  to  the  sphincter. 

Without  attempting  to  decide  this  dispute,  I  shall  re- 
strict m.yself  to  mentioning  that  I  certainly  obsei'ved  in  a 
few  of  my  cases  changes  in  the  orificium  corresponding 
to  the  description  of  Busch.  In  this  respect  case  7  is 
most  characteristic.  The  changes,  however,  were  at  the 
same  time  combined  with  other  deviations  in  the  orificium 
and  in  the  prostatic  urethra.  For  this  reason  they  have, 
according  to  my  opinion,  only  a  subordinate  importance 
so  long  as  the  prostate  enlargement  remains  within  at 
least  moderate  limits.  I  am  not  competent  to  decide  to 
what  extent  Busch's  theory  is  sufficient  to  explain  the 
phenomena  of  cases  that  have  extensive  prostate  enlarge- 
ment, because  I  never  saw  pure,  uncomplicated  cases  of 
this  kind.  At  any  rate,  it  seems  to  me  that  the  "mechan- 
ism" of  Busch  occurs  not  too  frequently,  and  when  it  oc- 
curs it  is  hardly  the  only  cause  of  Ischuria. 

According  to  it,  a  very  important  meaning  must  be 
given  to  the  so-called  "valve-mechanism""  in  the  develop- 
ment of  urine  retention,  provided  that  aside  from  it,  as  I 
have  explained  before,  other  causative  factors  display 
their  effects.  I  believe  that  these  valve-mechanisms,  of 
whatever  kind  they  may  be,  are  at  play  more  frequently 
than  is  generally  assumed,  inasmuch  as  thev  probably 
come  into  action  also  ift  the  cases  of  so-called  "general 
uniform  hypertrophy,"  and  apparently  are  missing  only 
at  the  isolated  enlargement  of  both  lateral  lobes.  If  we 
add  the  cases  of  general  uniform  prostate  enlargement  of 
all  three  lobes  to  those  in  which,  aside  from  the^  enlarge- 
ment of  both  lateral  lobes,  a  greater  hypertrophy  of  the 

71 


"middle"  lobe  is  observed,  we  shall  have  then  a  group  to 
which  the  same  opportunity  of  a  development  for  ihe 
valve-mechanism  is  given  as  in  the  isolated  enlargement 
of  the  middle  lobe  alone.  A  second  group  will  be  formed 
by  all  those  cases  in  which  the  enlargement  is  expressly 
described  as  an  isolated  hypertrophy  of  both  lateral  lobes 
without  an  active  participation  of  the  middle  lobe, 
whereby  we  shall  not  take  into  account  whether  both 
lateral  lobes  are  uniformly  or  irregularly  enlarged.  By 
this  means  the  following  compilation  is  formed  : 


No.  of 
cases 

ThOMP?ON             125 

MOTZ  (Sga)          60 

IVERSEN  (64)        52 

My  own  cases     iS 

of  all  three  lobes 
of  the  middle  lobe  a 
98 
34 
31 
15 

or 
lone 

Enlargement 
Isolated  (enlargement) 
of  both  lateral  lobes 

It 
21 

3 

The  Anterior 
commissure 
3 

Total                  255 
or  per  cent 

178 
69.8 

74 
29.1 

3 
I.I 

In  the  more  extensive  statistics  cited  are  contained  also 
the  cases  of  Messer  (94),  Guyan  (40,  Ed.  2,  1885,  p.  121) 
and  Launois  (72).  The  casual  contributions  scattered  in 
the  literature  are  hardly  needed  for  our  purpose,  and  for 
this  reason  were  not  used.  However,  the  following  com- 
pilation of  Iversen  (1.  c.  p.  32)  may  here  be  cited  indi- 
vidually : 

Thompson  &  Messer    IvERSE^f 
from  49  cases  52  cases 

Hypertrophy  of  the  Prostate  (without  more  definate  marks)    34.7  per  cent        25.0  per  c. 
All  3  Lobes  Enlarged  36.6        "  26.9    " 

Isolated  enlargement  of  both  lateral  lobes  32.7         "  40.4     " 

"  ■•  "  the  middle  lobe  2.0         "  7.7     " 

From  this  compilation  it  will  be  seen  that  during  the 
course  of  a  disturbance  in  micturition  during  lifetime  the 
valve-mechanism  exists  in  at  least  one-third  of  the  cases. 
Key  and  Santesson  (126)  also  believe  that  this  mechan- 
ism is  more  frequently  formed  than  can  be  assumed  on  a 
basis  of  the  statistical  compilations. 

In  what  way  the  valve-mechanism  is  formed  is  not 
estabhshed  with  sufficient  clearness  up  to  the  present  time. 
Formerly  much  stress  was  laid  upon  the  so-called  mus- 
cular bladder-neck  valves.  By  some  these  muscular 
valves  are  described  as  polypoid  myomata  of  the  pos- 
terior lip  of  the  orificium ;  others,  especially  the  old 
French  aiithors  (Alercier  [92]),  define  them  as  trans- 
verse (or  oblique)  or  crescent-shaped  folds  or  pads,  cov- 

72 


ering  the  posterior  division  of  the  orificium  and  formed 
by  the  hypertrophic  "sphincter." 

As  a  second  kind  of  bladder-neck  valves,  all  those  more 
or  less  movable  tumors  are  described  which  contain  in 
their  interior  a  certain  quantity  of  gland  tissue,  and  which 
take  their  origin  in  the  so-called  commisure  posterior,  or 
"Portio  intermedia,''  of  the  prostate  gland,  i.  e.,  in  that 
posterior  and  upper  part  of  the  prostate  gland  which  lies 
between  the  sphincter  and  the  vasa  differentia,  and  which 
connects  the  two  lateral  lobes  with  each  other.  As  is  well 
known,  the  middle  lobe  does  not  exist  in  the  normal 
condition.  That  part  of  the  prostate  which  lies  be- 
hind the  urethra  has  the  significance  only  of  a  posterior 
commisure,  so  that  all  tumors  observed  at  the  posterior 
lips  of  the  orificium  are  to  be  regarded  as  a  pathological 
phenomenon.  The  existence  of  the  muscular  bladder-neck 
valves  in  the  sense  of  Mercier  was  emphatically  denied  by 
Rokitausky   (112). 

Dittel  (23)  maintains  that  the  hypertrophic  middle  lobe 
does  not  project  behind  the  sphincter  into  the  lumen  of 
the  bladder,  but  originates  from  the  "portia  intermedia" 
in  front  of  the  sphincter,  and  encroaches  during  its 
growth  between  the  mucous  membrane  of  the  urethra  and 
the  posterior,  half-ring  of  the  sphincter;  by  which  pro- 
cedure the  sphincter  comes  to  lie  behind  as  a  tumor  func- 
tionating like  a  valve  (1.  c.  p.  147).  Neither  were  Mer- 
cier's  muscular  bladder-neck  valves  ("Barriere  vesicale") 
accepted  by  Dittel,  as  it  seems.  Also  Klebs  (305,  p.  1121) 
denies  any  pathological  importance  in  the  muscular  trans- 
verse ridges  of  the  orificium,  and  questions  the  existence 
of  the  "Barriere  vesicale."  Even  if  other  investigators 
do  not  go  so  far  (compare  Pitha  106,  p.  109),  the  con- 
viction prevails  generally  that  the  muscular  folds  of  the 
orificium  are  less  frequently  met  with  than  is  maintained 
by  Mercier. 

The  already  cited  view  of  Dittel  is  disputed  by 
Socin  (119,  p.  45),  who  is  of  the  opinion  that  the  sphinc- 
ter always  takes  a  part  also  in  the  formation  of  the  valve- 
like excrescence  of  the  orificium,  at  least  in  so  far  as  the 
hypertrophic  "portio  mediana"  displaces  the  muscles  up- 
ward and  forward.  Even  after  the  muscular  ring  is  in- 
filtrated with  the  glandular  tissue  and  partly  lost  (which 
process  will  be  considered  later  on),  the  posterior  segment 

73 


of  the  sphincter,  according  to  Socin,  still  remains  intact, 
and  expands  as  a  more  or  less  projecting  fold  (obstruct- 
ing the  outflow  of  urine)  between  the  lateral  lobes.  Also, 
according  to  Maas  (84,  p.  591),  Fenwick  (37)  and  Al- 
bert (i,  pp.  T92-194),  there  exists  a  purely  muscular 
valve,  "even  if,  perhaps,  it  seldom  occurs"  (as  is  added  by 
Albert).  The  authors  of  the  pathological-anatomical  and 
surgical  manuals  take  mostl_v  a  mediate  position  (com- 
pare in  this  respect,  for  instance,  Orth  310,  p.  298,  Till- 
manns,  128,  p.  369  [i]).  From  the  older  literature  I 
shall  also  cite  the  views  of  Virchow  (135),  because  he 
characterizes  most  clearly  the  different  subdivisions  of  the 
bladder-neck  valves  and  justly  differentiates  them  sharply 
one  from  another. 

Virchow  confirms  the  positicii  that  a  thickening  is 
sometimes  formed  in  the  muscular  bundles  of  the  bladder- 
neck,  which,  especially  in  old  people,  projects  in  the  form 
of  a  flat,  transverse  ridge,  the  so-called  "valvula  vesico- 
urethralis  se  sen  noula/'  which  also  hypertrophies  and 
thereb}'  interfere  with  the  micturition  and  catheterization 
(Barriere  vesicale).  This  is  to  be  sharply  differentiated, 
however,  from  the  so-called  "hypertrophic  middle  lobe," 
i.  e.,  from  the  myomatous  or  glandular  tumor  projecting 
from  the  posterior  circumference  of  the  orificium  ( 1.  c.  p. 
137).  These  tumors  are  generally  not  pure  myomata; 
"even  if  they  are  fibromuscular  for  the  greater  part,  we 
find  certain  segments  which  still  contain  glandular  struc- 
tures, from  which  a  certain  amount  of  epithelium  may 
be  exDressed  in  the   form  of    a  turbid,    whitish    fluid" 

(P-   138). 

The  incontinence  of  urine  was  generally  referred  to 
this  cause,  namely,  that  the  hypertrophic  "middle  lobe" 
projected  into  the  lumen  of  the  urethra  in  the  vicinity  of 
the  orificium,  and  thereby  made  the  orificium  incapable  of 
closing.  A  chief  representative  of  this  view  is  Dittel  (2^1), 
who  believed  that  he  saw  during  an  extensive  enlarge- 
ment of  the  "middle  lobe"  the  half-ring  of  the  sphincter 
assume,  when  displaced  upwards  and  backwards,  the  form 
of  a  thin,  flat'  muscular  layer,  hardly  visible  behind  the 
valve-like  tumors  and  therefore  with  insufficient  power  to 
close  the  urethra. 

This  contention  of  Dittel's  was  opposed  by  Socin  (119) 
and  Orth  (310). 


Socin  supports  his  theor}'  with  the  fact  that  in  most 
cases,  especially  in  a  high-grade  hypertrophy  of  the 
"middle  lobe,"  there  is  no  sign  of  a  sphincter  to  be  de- 
tected behind  the  latter,  even  in  the  form  of  a  very  thin 
and  flat  muscle  layer.  On  the  other  hand,  Socin  believes 
he  has  demonstrated  that  the  sphincter  is  not  only  pushed 
forwards  and  upwards  by  the  hypertrophic  "middle 
lobe,"  but  that  it  is  also  infiltrated  with  glandular  tissue, 
which  pushes  itself  between  the  muscle  bundles  of  the 
sphincter  and  through  the  middle  lobe;  and  at  last  the 
sphincter  is  entirely  destroyed  (1.  c.  p.  41).  The  orificium 
is  either  not  at  all  closed  (absolute  incontinence)  or  only 
passivelv  closed  (complete  retention)  by  the  valve-mech- 
anism (1.  c.  p.  45).  But  before  it  comes  to  either  of  these 
extremes  the  insufficiency  of  the  sphincter  and  the  ob- 
struction to  the  outflow  of  urine  may,  during  a  long 
period,  form  different  combinations. 

Guyon  takes  an  indifferent  position  as  regards  the  ex- 
planation of  the  involtmtary  outflow  of  urine,  inasmuch 
as  he  refers  it  to  the  extensive  fibrous  degeneration  of  the 
bladder  muscles,  which  also  ultimately  attacks  the 
sphincter. 

Lately,  Jores  (68),  has  occupied  himself  with  these 
questions.  His  work  closes  with  the  statement  that  the 
polypoid  bladder-neck  valves  have  nothing  to  do  with  the 
so-called  posterior  commissure,  or  "portio  intermedia"  oi 
the  prostate,  which  always  lies  behind  the  sphincter,  be- 
tween it  and  the  vas  deferns.  Such  valve-like  orificium 
tumors  are  akvays,  according  to  Jores,  composed  of  pros- 
tate tissue;  i.  c,  they  always  contain  besides  muscular 
tissues  also  glandular  tissue.  They  take  their  origin,  not 
from  the  prostate  gland  itself,  but  from  the  glandular 
tissue,  which  is  already  normally  present,  in  most  indi- 
viduals, above  the  colliculus  seminalis,  just  below  the  mu- 
cous membrane  of  the  urethra  and  orificium  respectively; 
at  any  rate,  in  front  of  the  sphincter. 

The  existence  of  this  glandular  collection  was  later 
demonstrated  also  by  Aschoff  (2). 

The  pediculator  valve-like  myomata  have  not  been  in- 
vestigated by  Jores  himself,  but  he  believes  that  the  myo- 
matous form  of  the  bladder-neck  valves  may  originate  out 
of  the  glandular  through  atrophy  of  the  gland  and  says : 
*'The  fibromuscular  form  must  be  related  in  its  develop- 


75 


ment  to  the  existence  of  glandular  tissue."  This  sen- 
tence is  synonimous  with  the  statement  of  Griffith's  (53), 
that  the  local  prostrate  hypertrophy  in  the  neighborhood 
of  the  orificium  internum  is  only  when  the  glandular 
tissue  was  already  present  above  the  colliculus  seminalis 
in  the  vicinity  of  the  latter  middle  lobe.  In  the  descrip- 
tions of  the  behavior  of  the  sphincter  during  the  highest 
degree  of  prostate  hypertrophy,  the  statement  of  Dit- 
tel,  that  the  sphincter  is  pushed  backward  and  upward 
was  at  last  confirmed  by  Jores.  On  the  other  hand,  he 
lays  stress  upon  the  agreeing  position  of  Socin  that  the 
sphincter  at  the  same  time  grows  through  the  glandular 
tissue  and  is  destroyed,  and  that  it  is  not  at  all  to  be 
found  posteriorly  above  (1.  t.  p.  233). 

In  agreement  with  Virchow,  one  must  sharply  limit 
the  "Barriere  vesicale"  of  Mercier,  i.  e.,  that  transverse 
fold  covering  the  orificium  form,  behind  which  it  is  un- 
doubtedly able  to  hinder,  to  a  great  extent,  the  free  out- 
flow of  urine  by  the  valve-like,  more  or  less  pedunculate 
tumors,  which  project  from  the  posterior  circumference 
of  the  orificium,  i.  e.,  from  the  bladder-neck  valves  of  the 
"sensu  stricto."  Among  the  latter  one  must  strictly  dif- 
ferentiate the  tumors  composed  chiefly  of  muscle  tissue 
from  the  tumors  composed  of  muscle  and  glandular 
tissue. 

The  existence  of  Mercier's  folds  is  by  no  means  to  be 
denied,  but  it  seems  to  me  that  they  are  not  of  frequent  oc- 
currence, because  I  had  opportunity  to  observe  them  in 
only  two  of  my  cases  (i  and  14).  From  such  observa- 
tions, those  cases  ought  to  be  differentiated,  in  which  the 
post,  lip  of  the  orificium  is  pushed  slightly  forward  and 
upward  by  the  enlarged  "portio  intermedia."  From  the 
sagittal  section  it  is  easy  to  establish  here  the  proposition 
that  the  sphincter  is  really  pushed  slightly  upward  and 
forward,  and  lies  just  beneath  the  mucous  membrane;  but 
in  front  of  this  membrane  either  there  are  an  accessory 
gland  (lores  and  Aschofif ),  or,  if  they  be  present,  at  least 
they  have  suffered  no  pathological  changes.  Such  a  con- 
dition is  illustrated  in  Table  VI. 

I  do  not  believe  that  a  similar  condition  is  of  serious  im- 
portance ;  it  is  in  my  opinion  pretty  insignificant  if  it  be 
present  without  additional  complications.  If  I  mentioned 
it,  it  was  only  because  it  more  easily  explains,  at  least  in 

76 


some  cases,  the  development  of  the  inabihty  to  close  the 
orificium,  with  the  assistance  of  other  conservative  factors. 
This  condition  has  only  a  superficial  similarity  to  Mer- 
cier's  bladder-neck  valve,  in  that  in  both  changes  the 
shpincter  lies  just  beneath  the  muc.  membr.  of  the  orifice. 
The  origin  of  the  Mercier  fold  is  not  explained  sufficiently 
up  to  the  present  time.  Of  the  attempts  at  elucidation 
which  refer  the  Mercier  fold  to  a  hypertrophy  of  the 
sphincter,  I  take  no  account ;  the  existence_  of  such  a 
hvpertrophy  is  not  proved  by  anybody,  and  it  is  on  the 
whole  hard  to  understand  how  such  a  hypertrophy  could 
originate.  Neither  is  a  clear  anatomical  picture  furnished 
by  the  statements  of  some  investigators  that  the  Mercier 
fold  is  a  "sphincter  stretched  between  the  lateral  lobes  of 
the  prostate."  It  has  long  been  known  that  the  prostatic 
urethra  is  pulled  longitudinally  during  a  hypertrophy  ex- 
tending in  a  sagittal  direction,  whereby  it  is  transferred 
from  a  small,  triangular  slit  into  a  long,  straight  line. 
This  change  in  the  form  of  the  urethra  has  its  cause, 
without  doubt,  in  that  the  hypertrophic  lateral  lobes  of 
the  prostate  enlarge  entirely  posteriorly  as  they  find  re- 
sistance in  front  at  the  symphysis,  to  which  they  are 
strongly  attached.  With  the  lateral  lobes  growing  in  the 
sagittal  direction,  the  lining  of  the  urethra  is  of  course, 
in  the  same  sense,  longitudinally  pulled.  If  now  there 
were  no  glands  present  in  the  neighborhood  of  the  ori- 
ficium in  front  of  the  sphincter,  or,  at  least,  if  they  suf- 
fered no  change,  and  if  the  portio  intermedia  was  not  en- 
larged to  a  higher  degree;  in  short,  if  in  the  lumen  of 
the  orifice,  either  in  front  of  or  behind  the  sphincter,  any 
pathological  excrescence  projects,  then  the  powerful  ring 
muscle  will  remain  more  or  less  normal  during  a  prostate 
hypertrophy  in  spite  of  the  changes  in  the  part  of  the 
prostatic  urethra  which  lies  outside  its  vicinity,  and  the 
orifice  itself  will  retain  its  normal  form.  It  is  proved: 
that  the  orifice  will  not  be  pushed  by  it  in  any  direction, 
because  the  anterior  half-ring  of  the  sphincter  is  strongly 
attached  to  the  symphysis,  and  the  prostate,  as  it  en- 
larges posteriorlv,  is  not  capable  of  pushing  it  away  from 
this  situation.  The  displacement  of  the  sphincter  pos- 
teriorlv (reallv  its  posterior  half-ring),  and  its  removal 
from  the  symphysis-and  anterior  bladder  wall  respectively 
would  only  be  possible  if  the  sphincter  were  pushed  apart 

77 


by  a  tumor  lying  zviiJiiii  the  orifice,  or  if  the  physiological 
tone  of  the  sphincter  were  overcome  by  a  posteriorly  di- 
rected pull  of  the  hypertrophic  prostate.  In  an  isolated 
hypertrophy  of  the  lateral  lobe  of  the  prostate,  this  oc- 
currence must  be  either  entirely  excluded,  in  view  of  the 
strength  of  the  ring  muscle,  or  must  at  least  be  regarded 
as  an  exceedingly  rare  exception. 

Therefore,  in  an  isolated  enlargement  of  both  lateral 
prostate  lobes,  neither  the  form  nor  the  situation  of  the 
orifice  will  be  changed.  Below  the  sphincter,  on  the 
other  hand,  to  which  the  effect  does  not  reach,  the  lining 
of  the  urethra  will  be  pulled  lengthwise  posteriorly  and 
will  have  the  form  of  a  slit. 

The  more  the  lateral  lobes  enlarges,  the  more  is  the 
lining  of  the  prostatic  urethra  pushed  behind,  beneath  the 
posterior  half-ring  of  the  sphincter.  Of  course  the  pos- 
terior lip  of  the  orifice,  which  contains  only  the  posterior 
half-ring,  will  in  this  way  form  a  transverse  fold,  which 
comes  to  lie  above  the  lining  (pulled  from  behind),  of  the 
urethra. 

It  is.  in  m.y  opinion,  not  necessary  to  consider  in  this 
regard  the  unfounded  hypothesis  of  a  hypertrophy  of  the 
ring  muscle,  nor  to  assume  that  a  special  stretching  of  the 
sphincter  between  the  lateral  lobes  of  the  prostate  takes 
place. 

On  the  contrary,  the  Mercier  fold  is  found  only  when 
the  prostatic  urethra  beneath  the  ring  muscle  is  changed, 
while  the  behavior  of  the  latter  is  still  normal.  Yes, 
furthermore,  it  is  found  only  because  the  sphincter  re- 
mains normal. 

The  Mercier  "valve-mechanism,"  in  the  true  sense  of 
the  word  (Barriere  vesicale),  has,  therefore,  as  a  sequel 
only  an  increase  in  the  curvature  of  the  urethra. 

I  have  mentioned  before  that  the  catheterization  is  just 
as  much  interfered  with  and  the  disturbance  of  micturi- 
tion is  just  as  easily  produced  by  the  Mercier  fold  as  by 
the  real  valve-mechanism. 

If  one  wishes  to  include  the  Mercier  fold  in  the  patho- 
genesis of  retention  of  urine  in  the  sense  of  a  bladder-neck 
valve  in  a  tinder  meaning  of  the  words,  nothing  is  to  be 
said  against  it ;  in  this  sense  we  must  admit  that  also  in 
isolated  enlargement  of  the  lateral  lobes  the  valve-mechan- 
ism may  sometimes  play  a  role. 

78 


More  exactly  and  better  than  the  foregoing  analysis 
the  drawings  Figs.  6  and  8  in  Tables  VI.  and  VII.  illus- 
trate the  formation  of  Mercier's  fold. 

As  regards  .the  real  "bladder-neck  valves."  i.  e.,  the 
pedunculated  tumors  of  the  posterior  lip  of  the  orifice,  I 
am  not  able  to  decide  whether  such  tumors  are  sometimes 
really  true  myomata,  free  from  glandular  tissue,  because 
I  never  met  with  a  single  similar  case  during  my  investi- 
gatiou.  Of  course  "a  priori"  it  cannot  be  denied  that 
true  mvomata  may  originate  in  the  vicinity  of  the  ori- 
fice just  as  well  as  in  other  parts  of  the  organism,  where 
they  take  their  origin,  either  from  pre-existing  muscular 
tissue  or  from  scattered  blyastodermic  membrane. 

Still  it  seems  to  me  that  such  true  myomata  of  the  ori- 
fice, free  from  glandular  tissue,  is  a  very  great  rarity. 
All  the  later  authors  lay  stress  especially  upon  the  state- 
ment that  they  saw  more  or  less  abundant  glandular  tissue 
in  the  apparent  myomata  (under,  if  not  with  the  naked 
eve,  then  at  least  the  microscope).  ( Klebs  [305],  Socin 
[119],  Griffiths  [53],  Jores  [68],  and  others). 

The  cases  in  which  true  myomata  of  the  orifice  were  ap- 
parently met  with  date  back  to  a  time  during  which  histo- 
logical investigation  was  only  little  used,  and,  therefore, 
they  lost  their  entire  value.  I  have  already  cited  a  state- 
ment of  Virchow,  made  in  1863,  from  which  it  will  be 
.seen  that  this  greal  investigator  has  demonstrated  the 
presence  of  glandular  epithelium  in  the  vicinity  of  the 
myom.ata  of  the  orifice.  Truly  only  a  single  myoma  of 
the  orifice  was  especially  mentioned  by  Virchow.  Of  this 
he  said :  "  .  .  .  glandular  tissue  was  not  contained 
in  it."      (1.  c.  p.  138). 

Even  in  this  case  the  microscopical  investigation  is  not 
especially  m_entioned ;  therefore,  it  also  is  not  freed  from 
objection.  In  spite  of  careful  search,  I  did  not  find,  in  all 
the  literature  within  reach,  another  case  of  myoma  free 
from  objection. 

In  all  my  observations  in  which  I  found  pedunculated 
tumors  in  the  orifice,  I  could  demonstrate  with  the  mi- 
croscope that  for  tile  greater  part  they  consisted  oi 
glandular  tissue.  In  this  regard  I  can  absolutely  testify 
the  view  of  Jores.  These  glandular  tumors  always  had 
their  seat  in  front  of  the  posterior  half-ring  of  the  sphinc- 
ter, just  beneath  the  muc.  membr.,  and,  therefore,  in  a 

79 


place  where  glandular  tissue  is  often  found  normally.  In 
my  opinion,  there  is  no  doubt  that  just  these  accessory 
glandular  groups  are  really  to  be  regarded  as  the  point  of 
origin  for  those  pedunculated  excrescences.  The  state- 
ment of  Jores  that  these  orifice  tumors  have  nothing  to  do 
with  the  posterior  commisure  of  the  prostate  ("portio 
intermedia")  seems  to  me  to  be  correct. 

Let  us  now  turn  to  the  involuntary  outflow  of  urine, 
and  the  role  which  the  ring  muscle  plays  in  regard  to  this. 
Of  the  prevailing  views  of  this  matter  no  one  seems  to  me 
to  be  absolutely  correct.  Either  of  them  can  only  ex- 
plain a  certain  group  of  cases ;  neither  suffices  as  an  ex- 
planation of  all  the  cases  of  incontinence.  It  is  without 
doubt  that  the  cause  of  incontinence  is  always  to  be 
sought  in  the  failure  of  the  sphincter  to  contract.  All 
the  investigators  are  entirely  unanimous  in  this  respect. 

In  those  rare  cases  in  which  sphincter  insufficiency  is 
not  accompanied  by  an  enlargement  of  the  prostate  (the 
so-called  "prostatisure  vesical"),  the  condition  of  incon- 
tinence could  only  be  referred  to  the  changes  in  the 
stricture  of  the  sphincter  itself,  as  Guyon  thought  it 
should  be.  The  structural  changes  of  the  sphincter  are 
in  all  probability  analogous  to  those  which  take  place  in 
the  bladder  wall,  as  already  described  in  the  first  part  of 
my  work;  and  here^  as  well  as  there,  they  are  not  to  be 
referred  to  arterial  schrosis,  but  to  a  simple  atrophy  of 
the  bladder  muscle.  The  strength  of  the  sphincter  sur- 
rounding the  orifice  gives  a  sufficient  explanation  why 
these  structural  changes  of  the  sphincter,  which  probably 
go  hand  in  hand  with  the  structural  changes  in  the  blad- 
der wall,  nevertheless  produce  their  injurious  effect  much 
later  than  these.  Here,  as  well  as  in  the  bladder  wall,  the 
chronic  inflammatory  complications  may  take  a  part  in 
the  formation  of  changes,  and  thereby,  as  they  cause  an 
active  proliferation  of  the  con-tis.  framework,  they  may 
increase  the  serious  consequences  of  the  atrophic  process. 
Also  in  the  cases  in  which  a  so-called  "Prostate  hyper- 
trophy" is  present,  similar  pathological  processes  prob- 
ably play  a  certain  role,  especially  where  no  high-grade 
form  of  change  in  the  orifice  exists. 

But  when  the  latter  are  also  involved,  these  processes 
have  generally  only  a  subordinate  importance. 

I  cannot  quite  understand  why,  to  some  investigators, 

80 


Mecier's  old  explanation  of  ithe  incontinence  of  urine  ap- 
pears to  be  wrong  and  forced ;  to  me,  for  a  certain  group 
of  cases,  it  has  by  no  means  lost  its  value. 

The  tumors  situated  on  the  posterior  lip  of  the  orifice 
project,  as  a  rule,  only  to  a  certain  extent  beyond  the 
orifice  into  the  interior  of  the  bladder ;  but  if  they,  in  their 
early  growth,  or  right  from  the  start,  force  themselves 
into  the  lumen  of  the  orifice,  whereby  the  latter  is  deformed 
and  the  sphincter  pushed  apart,  then  the  function  of  the 
sphincter  must  certainly  suffer  damage. 

Under  such  circumstances  the  time  at  which  the  urine 
begins  to  flow  involuntarily  depends  entirely  on  the  con- 
dition of  the  muscles  of  the  bladder  wall,  as  these  are,  to 
a  certain  extent,  antagonistic  to  the  sphincter. 

If  during  the  time  of  the  functional  ability  of  the 
sphincter  this  is  interfered  with  by  an  interposing  tumor 
and  the  bladder  wall  still  retains  its  normal  structure,  then 
the  incontinence  will  be  developed  very  quickly.  If  on 
the  contrary  the  bladder  wall  be  atrophic,  then  the  be- 
ginning of  the  incontinence  will  alwa3^s  occur  at  a  later 
period,  according  tO'  the  structural  changes  in  the  bladder 
wall,  which  on  their  side  give  rise  to  a  retention  of  urine, 
because  the  sphincter,  although  interfered  with  in  its 
function,  is  capable  for  a  certain  time  of  working  against 
the  bladder  wall,  which  is  just  as  weak,  and  is  able  to 
maintain  the  physiological  equilibrium.  If,  lastly,  the 
elasticity  and  contractility  of  the  bladder  wall  be  almost 
entirely  lost  in  consequence  of  very  extensive  structural 
changes,  then,  "ceteris  paribus,"  the  incontinence  will  oc- 
cur very  late  and  only  after  the  bladder  is  dilated  to  its 
utmost  limit  and  its  inelastic  and  non-contractile  walls 
exert  a  passive  resistance  to  a  further  dilatation. 

Thus  even  comparatively  small  tumors  may  produce 
greatly  differing  degrees  of  incontinence,  from  the  sim- 
ple incontinence  to  a  true  "Ischuria  paradoxa,"  providing 
that  they  project  into  the  lumen  of  the  orifice.  The  in- 
continence is  "ceteris  paribus"  more  easily  produced,  the 
more  the  tumor  situated  in  the  orifice  enlarges ;  i.  e.,  the 
wider  the  muscular  ring  is  pushed  apart,  the  more  will  its 
function  be  interfered  with  and  the  more  extensively  will 
the  orifice  be  deformed.  In  such  cases  the  posterior  half- 
ring  of  the  sphincter  is  always  pushed  behind,  as  observed 
by  Dittel  and  verified  by  Jores.     I  have  also  verified  this 

8r 


by  my  own  investigation  of  insignificant  and  moderately 
large  tumors  of  this  kind. 

With  a  large  tumor  of  this  kind  it  is  hardly  possible  to 
find  a  sphincter  at  the  place  indicated  by  Dittel  and  in  the 
form  described  by  him.  In  this  regard  the  statement  of 
Socin  is  correct,  inasmuch  as  behind  the  greater  tumors 
there  is  really  no  sign  of  a  sphincter  half-ring  to  be  de- 
tected. This  fact  was  also  observed  by  Jores,  since  he 
found  no  sufficient  explanation  in  his  cases  which  would 
correspond  to  the  views  of  Dittel  he  resorted  to  Socin's 
theory,  according  to  which  the  sphincter  is  entirely  de- 
stroyed by  the  ingrowing  new-formed  glandular  tissue. 
From  my  own  experiences  I  can  verify  the  facts  ob- 
served by  Dittel  as  well  as  the  discoveries  of  Socin ;  yet 
with  the  restriction  that  the  former  are  observed  only  in 
the  insignificant  and  moderate,  the  latter  exclusively  in  the 
higher  degrees  of  tumors  which  push  apart  the  orifice. 
On  the  other  hand,  I  cannot  possibly  affirm  the  general 
conclusions  drawn  from  the  observations  of  both  these 
investigators;  neither  can  I  join  in  the  mediate  explana- 
tion of  Jores.  By  the  investigation  of  the  starting  period 
and  of  the  moderate  prostate  hypertrophy,  I  was  con- 
vinced that  the  glandular  tissue  present  in  the  enlarged 
parts  of  'the  prostate  never  projects  between  the  muscle 
bundles,  and,  too,  it  neither  infiltrates  the  sphincter  nor 
destroys  it. 

The  borders  of  the  sphincter  are  always  in  a  cross-sec- 
tion in  a  straight  line  and  sharply  defined ;  they  are  never 
uneven  nor  indistinct.  On  the  other  hand,  it  seems  to  me 
that  without  doubt  the  posterior  sphincter  half-ring  which 
is  entirely  free  from  glandular  tissue  is  simply  pushed 
upward  from  below  and  behind  by  the  hypertrophic  "por- 
tio  intermedia,"  and  from  below  and  in  front  by  the  grow- 
ing submucous  tumor.  Of  course  this  can  only  happen 
when  not  only  the  submucous  tumor,  but  also  the  true 
"portio  intermedia"  enlarges.  That  is  in  the  cases  in 
which  there  really  exists  a  general  "prostate  hypertrophy." 
The  post,  sphincter  half-ring  has,  in  a  sagittal  section,  the 
form  of  a  sharp  wedge,  the  apex  of  which  points  down- 
wards, and  the  ant.  border  of  which  lies  normally  just  be- 
neath the  mucous  membrane  of  the  orifice  and  the  pos- 
terior part  of  the  prostatic  urethra  (excluding  the  ac- 
cessory glands),  and  the  posterior  bower  of  which  is 

82 


touched  by  the  "portio  intermedia"  and  its  short  basis  is 
related  to  the  post  wall  of  the  bladder.  The  perpendicular 
which  connects  the  base  of  the  wedge  with  the  apex  re- 
mains unchanged  as  long  as  no  pathological  tumors  press 
upon  the  anterior  and  posterior  surface  of  the  prismatic 
muscular  half-ring.  It  remains  unchanged  even  when  the 
"portio  intermedia"  is  moderately  enlarged.  When  now 
a  glandular  tumor  develops  beneath  the  mucous  mem- 
brane of  the  orifice  and  when  the  "portio  intermedia" 
begins  at  the  same  time  to  enlarge,  and  when  later 
the  tumors  growing  on  either  side  and  beneath  the 
sphincter  take  on  greater  dimensions,  then  it  is  easy  to 
demonstrate  macnescopically  as  well  as  microscopically 
that  the  wedge-shaped  cross-section  of  the  sphincter  be- 
comes more  blunt  and  shorter,  whereby  its  borders  lose 
nothing  of  their  distinctiveness. 

By  the  pressure  of  the  growing  tumors  the  sphincter 
visibly  changes  its  form,  is  pushed  upward  and  projects 
slowly  above  the  level  of  the  original  orifice.  The  two  tu- 
mors which  push  the  sphincter  upward  approach  each  other 
slowly  and  finally  coalesce  into  a  single  mass.  The  pos- 
terior half-ring,  which  is  always  pushed  higher,  comes 
little  by  little  to  lie  in  the  neighborhood  of  the  bladder 
wall  proper. 

Finally  we  see  the  pictures  observed  by  Socin ;  i.  c,  the 
sphincter  apparently  exists  no  more. 

If  one  does  not  know  the  origin  of  such  pictures,  it  is 
easy  to  confound  the  deformed  and  displaced  posterior 
half-ring  of  the  sphincter  with  a  component  of  the  pos- 
terior bladder  wall  (or  rather  the  base  of  the  bladder). 
And  yet  the  sphincter,  from  an  anatomical  standpoint,  is 
not  lost,  and  all  the  muscle  bundles  which  compose  it  are 
still  retained. 

From  a  physiological  standpoint,  to  be  sure,  the  sphinc- 
ter does  not  exist  any  more  because  in  this  form  and  in 
this  place  it  cannot  functionate  normally;  whereby  the 
orifice  is  made  entirely  incapable  of  closing.  "If  the 
bladder  still  be  closed,  sometimes  in  such  cases  it  is  be- 
cause a  passive  valve-mechanism  is  eventually  present;" 
as  Socin  rightly  says  (1.  c.  p.  45),  although  he  gives  no 
specific  anatomical  reason  for  it.  The  Socin  theory,  in 
other  words,  stands  in  opposition  to  the  prevailing  be- 
havior of  the  "hypertrophic"  prostate  gland,  inasmuch  as 

83 


Socin  assumes  that  the  sphincter  is  destroyed  by  the 
glandular  tissue  he  alleges  that  hypertrophy  of  the  pros- 
tate gland  has  the  nature  of  a  malignent  adenoma,  with 
which  the  hypertrophy  of  the  prostate  has  really  nothing 
to  do. 

The  ways  and  means  by  which  the  different  symptoms 
of  senile  bladder  insufficiency  are  formed,  whether  it  be 
with  or  without  an  existing  prostate  enlargement,  have 
been  discussed  several  times  in  this  work.  As  I  have 
only  touched  upon  the  contested  points,  so  far  as  in  my 
investigation  material  was  found  for  their  elucidation,  the 
representation  of  the  symptomatology  of  the  senile  blad- 
der insufficiency  could  not  be  executed  either  systematic- 
ally or  exhaustively.  The  attempt  would  also  have  been 
unnecessary,  because  an  exhaustive  statement  may  be 
found  easily,  not  only  in  the  excellent  monograph  of 
Socin  Thompson,  etc.,  but  also  in  every  thorough  manual 
of  surgery. 

It  was  my  aim  to  call  attention  to  a  few  anatomical  pe- 
culiarities based  upon  my  own  investigations. 

Therefore,  I  must  put  aside  the  question  whether  the 
clinical  picture  of  "prostatismus,"  drawn  by  Guyon's 
master  hand  is  really  constant  or  at  least  to  be  observed  as 
a  rule.  I  could  at  most  resort  to  Socin's  authority,  as  this 
investigator,  in  his  excellent  monograph,  describes  dif- 
ferent clinical  pictures  of  the  "Prostatismus"  and  leaves 
unmentioned  a  constant  series  of  clinical  symptoms.  Only 
a  short  time  ago  he  stated :  'T  do  not  believe  that  a  'Pros- 
tatiker,'  in  the  sense  of  Guyon,  exists."^ 

As  I  have  no  right  to  decide  this  purely  clinical  ques- 
tion, I  must  limit  myself  to  the  investigation  whether  the 
Guyon  picture  of  the  "prostatismus"  can  be  sufficiently 
sustained  from  an  anatomical  standpoint,  by  the  results  of 
my  investigation. 

Really  only  one  point  is  involved,  namely,  the  explana- 
tion of  in  what  way  the  incontinence  can  occur  after  re- 
tention of  urine. 

The  succession  in  which  the  retention  of  urine  appears 
after  the  insignificant  beginning  of  disturbance  of  mic- 
turition is  exhaustively  explained  on  the  one  hand  by  the 
structural  changes  of  the  bladder  wall,  and  on  the  other 
by  the  pathological  changes  of  the  orifice  and  the  pros- 
tatic  urethra.     Regarding  the  question   why   sometimes 

84 


before  the  period  of  retention  of  urine  a  quickly  disap- 
pearing incontinence  of  urine  is  to  be  observed,  partly  it 
has  been  answered  already,  for  instance,  by  the  work  of 
Socin  (1.  c.  p.  56)  ;  and  partly  it  may  easily  be  dismissed 
on  account  of  my  previous  discussion. 

If  the  incontinence  of  urine  follows  the  retention  of 
urine  in  cases  in  which  the  prostate  is  not  all  enlarged  and 
no  signs  of  any  valve-mechanism  are  to  be  observed  in  the 
orifice,  then  this  phenomenon  can  be  explained  in  only  one 
way ;  that  is,  it  must  be  referred  to  the  structural  changes 
in  the  sphincter.'  But  it  must  be  taken  into  considera- 
tion that  if  these  structural  changes  in  the  vicinity  of  the 
bladder  wall  and  the  sphincter  develop  parallels  to  one 
another,  then  the  relative  proportion  of  the  function  of 
both  muscles,  which,  to  a  certain  extent,  act  antagonistic- 
ally to  each  another,  must  remain  unchanged  for  a  long 
time,  even  though  the  absolute  function  of  each  of  the 
muscles  may  have  suffered  greatly. 

As  I  have  mentioned  before,  and  as  is  generally  recog- 
nized, the  changes  in  the  prostatic  urethra  are  capable, 
without  the  assistance  of  the  valve-mechanism,  of  pro- 
ducing at  least  partial  retention  of  urine. 

The  bladder-muscle,  which  is  continually  more  and 
more  altered,  offers  to  the  residual  urine,  which  con- 
tinually becomes  weaker  and  weaker,  whereby  the  bladder 
gradually  becomes  more  and  more  dilated,  and  is  finally 
dilated  to  its  maximum  and  overfilled;  and  there  is 
formed  solely  through  the  passive  resistance  of  its  wall  a 
ture  "Ischuria  paradoxa." 

Under  such  circumstances  the  "Ischuria  paradoxa"  will 
be  formed  the  earlier  the  sooner  the  structural  changes  in 
the  bladder  wall  reach  their  maximum,  whereby  the  dila- 
tation of  the  bladder  reaches  its  uttermost  limit.  But,  be- 
cause the  time  at  which  the  structural  changes  of  the  blad- 
der wall  develop  depends,  among  other  things,  upon  the 
degree  of  the  obstruction  hindering  the  outflow  of  urine, 
as  I  have  explained  before,  the  degree  of  the  change  of 
the  prostatic  urethra  may  also  be  of  importance  for  the 
beginning  of  the  incontinence.  The  more  extensive  they 
are,  "ceteris  varvus,"  the  more  quickly  will  the  amount  of 
residual  urine  increase.  Quite  different  is  the  matter  in 
cases  of  "valve-mechanism"  in  the  true  sense  of  the  word ; 
in  such  cases  the  incontinence  may  be  developed  much 

85 


earlier,  even  before  the  dilatation  of  the  bladder  has 
reached  its  utmost  limit,  because  quite  different  influences 
are  at  work  here.  They  are  the  previously  described 
changes  in  the  sphincter,  which  directly  cause  the  inability 
of  the  orifice  to  close  and  cause  the  posterior  half-ring  of 
the  sphincter  to  lie  above  the  level  of  the  orifice  proper. 
The  change  in  the  valve-mechanism  in  such  a  condition  is, 
at  least  in  part  of  the  cases,  easy  to  understand.  The 
tumor  lying  between  the  mucous  membrane  and  the  sphinc- 
ter, as  was  first  demonstrated  by  Jores,  takes  its  origin 
from  the  accessory  prostatic  glandular  tissue  scattered  be- 
neath the  mucous  membrane  of  the  posterior  lips  of  the 
orifice.  As  long  as  the  groups  of  glands  enlarge  that  lie 
in  the  upper  division  of  this  part,  the  growing  tumor  will 
project  only  into  the  interior  of  the  bladder;  but  if  this 
process  also  attacks  the  inferior  division  and  extends  for- 
ward in  the  neighborhood  of  the  lumen  of  the  orihce 
proper,  then  the  tumor  begins  to  project  anteriorly  into 
the  lumen  of  the  urethra,  whereby  the  opening  of  the 
orifice  is  deform.ed  and  the  sphincter  pushed  apart.  It 
will  now  depend  on  the  form  and  size  of  the  tumor 
whether  the  valve-mechanism  is  partly  to  be  retained,  at 
any  rate  without  closing  the  orifice  as  promptly  and  ex- 
actly as  before,  or  whether  it  will  entirely  lose  its  effect. 
The  time  at  which  the  incontinence  appears  will  now 
mainlv  depend  upon  the  condition  of  the  bladder  wall. 

I  believe  I  can  now  sav  that  the  results  of  my  investiga- 
tion are  proved  to  be  sufficient  for  the  explanation  of  the 
clinical  picture,  as  characterized  by  Guycn. 


86 


CHAPTER    VIII. 

PATHOLOGICAL      HISTOLOGY      OF    THE     S0= 

CALLED    "PROSTATIC    HYPERTROPHY" 

AND    PROSTATIC    ATROPHY 

The  nature  of  the  process  to  which  the  name  "prostatic 
hypertrophy"  is  generally  given  has  been  defined  in  dif- 
ferent ways,  according  to  whether  the  one  or  the  other  of 
the  observed  pathological  changes  was  taken  up  as  the 
main  issue.  There  has  been  a  great  difference  of 
opinion,  although  the  characteristics  of  the  histological 
changes  were  represented  in  the  same  way  by  the  authors. 

Some  investigators  take  no  account  of  the  decision  of 
the  question  whether  the  name  "hypertrophy"  really  fits 
for  the  enlargement  of  the  prostate  occurring  during  ad- 
vanced age.  This  is  especially  so  in  the  older  works  (for 
instance,  Pitha  [io6])  ;  but  in  most  old  works  as  neither 
an  exact  representation  is  furnished  of  the  histo-patho- 
logical  changes,  nor  the  views  of  the  structure  of  the  nor- 
mal prostate  are  correct,  no  notice  of  these  wroks  need  be 
taken. 

The  opinion  of  many  modern  authors  is  analogous  to  the 
older  views,  since  they  regard  the  "hypertrophy"  of  the 
prostate  as  a  kind  of  physiological  senile  process  or  as  a 
physiological  involution.  The  latter  opinion  is  also  closely 
related  to  the  view  that  the  development  of  the  prostate 
progresses  parallel  with  the  development  of  the  testicle, 
and  that  it  is  in  this  parallelism  that  the  cause  of  a  "hyper- 
trophy" of  the  prostate  is  to  be  sought.  This  view  is  also 
in  intimate  relation  to  the  representation  originated  by 
Launois  (72,  73)  of  the  histology  of  the  "senile"  and  the 
"hypertrophic"  prostate.  Together  with  other  teachings 
of  tlie  Parisian  schools,  it  found  a  very  extensive  circula- 

8-7 


ticn  throf.^h  Giiyon's  works. 

Liunois  {y2)  rinas  no  sharp  distinction  between  the  so- 
called  "diffuse''  form  of  prostate  hypertrophy  and  the 
true  prostate  adenoma.  According  to  him,  a  "hyper- 
trophy" of  the  prostate  is  to  be  regarded  as  the  nodular 
form  (1.  c.  p.  87).  Aside  from  the  works  of  Launois 
there  are  none  in  which  it  is  not  demonstrated  tJiat  "hy- 
pertrophy" of  the  prostate  occurs  as  well  in  a  nodular  as 
in  a  diffuse  form.  These  nodules,  i.  e.,  the  easily  enu- 
cleated tumors,  develop,  according  to  Launois,  constantly 
beween  the  forty-fifth  and  the  fiftieth  year  of  life  during 
the  course  of  the  physiological  development  of  the  pros- 
tate ;  on  account  of  their  structure,  Launois  proposes  to 
call  these  nodules  "adeno-fibromyomes,"  or  "fibromes 
glandulaires"  (1.  c.  p.  77-81'. 

The  origin  of  these  nodules  is  to  be  referred  to  the  con- 
nective-tissue in  the  neighborhood  of  the  glandular  tubules. 
"Dans  le  prostate  des  viellards,  il  se  passe  un  veritable 
travail  de  sclerose  annulaire"  (1.  c.  p.  79).  This  hyper- 
trophy of  the  prostate  may  be  a  consequence  of  the  in- 
crease and  enlargement  of  these  nodules  "normally"  pres- 
ent (comp.  1.  c.  pp.  87-89).  The  supposed  connection  be- 
tween the  "hypertrophy"  of  the  prostate  by  "sclerose  an- 
nulaire" to  arterial  sclerosis  I  have  already  refuted  in 
the  first  part  of  my  work.  Launois  still,  ten  years  later, 
upholds  his  view  (which  in  the  main  was  accepted  by 
Guyon  [85,  pp.  105,  106])  without  making  further  in- 
vestigation (73  p.  730). 

Bv  the  great  majority  of  other  investigators  the  "hyper- 
trophv"  of  the  prostate  is  regarded  as  a  kind  of  new 
growth  (Neoplasm),  whereby  in  the  main  the  two  well- 
known  forms  of  this  process  are  differentiated,  the  my- 
omatous and  glandular ;  and  these  subdivided  into  a  nod- 
ular and  a  diffuse  form.  The  classification  cited  dates 
back  to  the  fundamental  works  of  Virchow  (135)  ;  but, 
although  thirty  years  have  elapsed  since  that  time,  we  have 
made  no  progress  in  research  in  this  pathological  condi- 
tion. The  idea  of  the  "hypertrophy"  of  the  prostate  gland 
as  a  neoplasmatic  process  "sensu  stricto"  was  perhaps 
most  thoroughly  worked  out  by  Cohnheim  (299  II,  p.  74), 
as  he  speaks  about  myomata  and  adenomata  without  any 
further  remark;  while  Thompson' ( 133,  pp.  80-81)  leans 
more  toward  the  older  views,  which  regarded  the  "pros- 


tatic  hypertrophy"  as  a  "genuine"  hypertrophy. 

Socin  (119,  pp.  30-31)  expresses  most  exacly  what  we 
should  understand  by  a  hypertrophy  of  the  prostate.  Ac- 
cording to  him,  this  is  a  collective  name  by  which  processes 
that  differ  somewhat  are  gathered  together,  inasmuch  as 
the  entire  enlargements  of  the  prostate  gland  which 
neither  have  an  inflammatory  origin  nor  a  malignant  new 
growth  (sarcoma  carcinoma)  are  meant  by  it.  At  any 
rate,  we  have  here  to  deal  with  no  genuine  'hypertrophy," 
but  with  a  tumefaction.  This  view  seems  to  be  most 
generally  accepted. 

The  description  of  both  main  forms  of  hypertrophy  of 
the  prostate,  the  myomatous  and  glandular,  is  repeated 
with  a  well-nigh  pedantic  monotomy  in  most  mono- 
graphs and  manuals  (Socin  [119],  Iversen  [64],  Maas 
[84],  Albert  [i],  Tillmans  [128],  Klebs  [305],  Birch- 
Hirschfeld  [297],  Orth  [310],  Kaufmann  [303],  Ziegler 
[314],  Jores  [68],  &c.,  &c.)  and  by  some  authors  the 
mixed  form  is  still  added  (Socin  [1.  c.  p.  37],  Orth  [1.  c. 
p.  299],  Kaufmann  [1.  c.  p.  668])  or  only  the  names  were 
changed  (Casper  [16,  p.  154]). 

For  this  reason  I  desist  from  the  description  of  these 
forms  in  the  sense  of  the  authors  cited ;  but  I  beg  to  be 
allowed  to  call  attention  to  the  difference  of  opinion  re- 
garding the  relative  frequency  of  the  individual  forms. 
Billroth,  for  instance,  thinks  (Discussion  of  Dittel's  Lec- 
ture [360] )  that  in  the  hypertrophy  of  the  prostate  the 
increase  of  glandular  tissue  never  plays  a  part ;  on  the 
other  hand,  the  hyperplasia  of  the  connective-tissue  and 
of  the  muscle  constantly  does. 

According  to  this  the  myoma  of  the  prostate,  since 
Virchow  (135,  p.  136),  is  regarded  by  most  of  the  in- 
vestigators as  a  phenomenon  at  any  rate  rare.  Socin  (119, 
p.  38),  Casper  (15,  pp.  154-155)  and  Jores  (68,  p.  240) 
have  not  a  single  case  of  a  genuine  myoma  of  the  pros- 
tate among  their  observations;  Motz  (89b,  p.  41)  cites 
only  a  single  corresponding  case.  Griffiths  (53)  assumes 
that  the  otherwise  verv  rare  genuine  myomata  are  to  be 
differentiated  principally  from  the  occurrence  of  a  hyper- 
trophv.  Also  those  investigators  who  lay  stress  upon 
the  observations  of  hypertrophy  of  the  prostate  with 
stronger  activitv  of  the  muscle  stroma  declared  particu- 
larly that  this  form  is  rarely  to  be  observed ;  or  they  set 

89 


up,  especially  in  the  more  recent  work,  the  hypothesis,  ac- 
cording to  the  example  of  Klebs  (Prag.  Viertel-jahr- 
schrift,  Bd.  124,  cited  in  305,  p.  1119),  that  this  form  is 
only  brought  about  during  the  later  stages  of  hypertrophy 
by  the  destruction  of  the  glandular  elements.  These 
views  find  their  verification  mainly  in  the  circumstance 
that  the  dififerent  forms  of  "hypertrophy"  of  the  prostate 
are  difficult  to  differentiate,  and  that  innumerable  transi- 
tional pictures  exist,  which,  according  to  my  opinion, 
point  to  the  conclusion  that  the  common  division  of  the 
"hypertrophy"  of  the  prostate  into  different  forms  and 
subdivisions,  is  forced  and  unjustified.  Some  inves- 
tigators go  still  farther  than  Klebs,  since  they  place  the 
origin  of  the  "prostate  hypertrophy"  of  all  forms  in  the 
glandular  tissue  alone.  Even  Virchow  (135)  expressed 
a  view  in  this  regard  which  was  overlooked  by  most  in- 
vestigators:  "According  to  my  opinion,  tJie  process  he- 
gins,  as  a  ride,  in  the  glandular  parts  and  connects  itself 
only  after  a  while  with  an  increase  in  the  stroma"  (1.  c.  p. 
135).  Nearly  at  the  same  time  Dodeuil  (22)  mentioned 
that  the  glandular  acini  in  the  hypertrophic  prostate  suffer 
an  enlargement  of  their  exterior  layer  of  the  walls  only  in 
consequence  of  an  extensive  formation  of  embryonal  con- 
nective-tissue elements.  The  echoes  of  such  views  are 
still  to  be  found  in  the  works  oi  Mausell-Moullin  (431) 
and  Griffiths  (53),  and  to  a  certain  extent  also  in  the 
works  of  Jores  (68).  The  views  of  Motz  ( [89b]  p.  42  f) 
are  related  to  those  of  Dodeuil. 

By  the  authors  cited  lastly  the  hypertrophy  of  the  pros- 
tate is  in  the  main  not  regarded  in  a  collective  sense,  but 
as  an  individual  disease  process,  and  its  different  forms 
as  different  periods  of  development  of  one  and  the  same 
process,  or  at  least  as  different  results  of  an  originally  in- 
dividual process. 

But,  as  well,  those  who  regard  the  "glandular"  form 
as  a  specific  subdivision  of  the  hypertrophy  of  the  pros- 
tate do  not  agree  as  to  where  in  such  cases  the  neoplas- 
matic  process  takes  its  origin.  A  few  authors,  as,  for  in- 
stance, Birch-Hirschfeld  ([297],  Bd.  II),  think  that  the 
epithelium  of  the  ghndular  tubules  plays  an  active  role 
in  the  new  formation  and  branching  of  new  solid  glandu- 
lar plugs  and  tubules.  However,  I  have  nowhere  found 
data  from  which  proof  can  be  obtained  for  the  new  for- 


90 


mation  and  sprouting  of  glandular  tubules.  Even  though 
the  proliferating  of  the  glandular  epithelium  be  men- 
tioned by  the  French  authors,  as,  for  instance,  Launois 
{72),  Guyon  (41),  Miquet  (87),  von  Motz  (896),  and 
in  addition  Cornie  and  Ravier  (298,  p'.  677),  yet  this  is 
to  be  solely  referred  to  the  pre-existing  alveoli  of  the 
gland  in  which  the  epithelium  is  said  to  proliferate  to- 
ward the  free  surface,  whereby  it  becomes  transformed 
from  a  single  layer  to  a  stratified  layer. 

Quite  differently  from  Birch-Hirschfeld  this  matter  is 
regarded  by  Rindfleisch  (311,  p.  581),  and  most  of  the 
authors,  as,  for  instance,  Orth  (310),  Albert  (i)  and 
Socin  ( 1 19,  p.  40)  follow  him  in  this.  The  starting  point 
of  the  new  growth  is  placed  by  these  authors  in  the  sub- 
epithelial connective  tissue,  and  this  proliferation  causes 
secondarily  an  enlargement  of  the  glandular  acini. 

The  histology  of  the  prostatic  atrophy  offers  much  less 
room  for  contention.  Furthermore,  up  to  the  present  day 
this  process  is  very  little  investigated.  Neither  did  the 
atrophy  of  the  prostate  awaken  much  practical  interest 
before  castration  was  proposed  as  a  treatment  for  "hyper- 
trophy" of  the  prostate. 

If  we  look  away  entirely  from  the  cases  of  eunuchs  and 
of  non-development  of  the  testicles  which  were  diligently 
gathered  from  the  literature  by  Launois  (73),  then  the 
atrophy  of  the  prostate  is  possibly  more  frequently  found 
in  old  people  than  the  so-called  "hypertrophy."  Socin 
(119,  p.  109)  states  that  atrophy  of  the  prostate  is  ob- 
served in  20-30  per  cent,  of  men  above  the  fiftieth  year  of 
life.  This  was  verified  by  Orth  (310,  p.  303),  Klebs  (05, 
p.  1 106),  Iversen,  anatomical  examination  (64,  pp.  15-17) 
and  Dittels,  clinical  examination  (23).  The  numbers 
given  by  Thompson,  two  per  cent,  atrophy  as  against 
twenty-two  per  cent,  hypertrophy,  are  undoubtedly  too 
low  an  estimate.  Among  the  twenty-one  old  people 
(without  hypertrophy  of  the  prostate)  whom  I  ex- 
amined, I  found  an  atrophy  in  nearly  one-half  of  the 
cases  (the  weight  below  13.5  grm.  As  a  well-charac- 
terized subdivision  the  local  focal  atrophv  of  the  pros- 
tate can  be  placed  beside  the  general  atrophy  of  the  pros- 
tate. To  the  first  may  be  added  the  cysts  of  the  prostate 
formed  by  dilatation  of  the  glandular  ducts,  due  to  an 
obstruction  to  the  outflow  of  the  secretion.     Such  cvsts 


91 


seem  to  be  of  very  rare  occurrence. 

Aside  from  the  observation  of  Cruveilhier  ( [300] 
Livv.  39  T.  2  f.  2),  who  saw  a  cystic  degeneration  of  the 
whole  prostate,  and  the  one  of  Enghsch  ([32]  p.  71), 
who  places  the  origin  of  the  submucous  cysts  of  the  "pars 
supramantana  prostatae,"  measuring  1.5x1.3  cm.,  in  the 
foetal  life  and  first  years  of  life,  respectively,  I  found  in 
the  literature  within  my  reach  only  one  case  of  Desnos 
(26)  and  Le  Dentu  (83).  Perhaps  we  may  include  here 
the  slit-like  recess  of  the  "pars  supramantana  prostatse" 
also  observed  by  Englisch,  which  was  possibly  formed  by 
a  destruction  of  the  anterior  wall  of  the  cysts  (1.  c.  p.  77). 
Klebs  (1.  c.  p.  1 106)  thinks  that  by  blocking  one  of  the 
glandular  ducts  with  amyfoid  bodies  a  cyst  may  be 
formed  in  the  prostate,  but  they  never,  as  a  rule,  reach 
such  a  size  as  to  be  diagnosticated  macroscopically.  In 
this  place  my  own  observation  might  be  cited  (case  60) 
as  to  a  few  cysts  measuring  as  much  as  8  m.m.  in  diam- 
eter, which  were  found  in  the  neighborhood  of  a  peduncu- 
lated orificial  tumor.  Aside  from  the  histological  investi- 
gations performed  by  Launois  in  the  hypoplastic  and 
atrophic  prostate,  respectively,  in  two  cases  of  Monorchis 
( [73]  P-  733)  a'^d  in  one  case  of  syphillitic  changes  in  both 
testicles  (1.  c.  p.  743),  I  was  not  able  to  find  corresponding 
data  in  the  literature  within  my  reach.  In  the  first  two 
cases  there  were  almost  no  glands  present  in  the  half  of 
the  prostate  corresponding  to  the  missing  testicle ;  in  the 
third  case  none  in  the  entire  gland.  The  atrophic  pros- 
tate of  old  people  were,  according  to  my  knowledge,  never 
histologically  examined  by  any  one.  Besides,  histological 
investigations  of  atrophic  prostates  after  castration  are 
not  numerous.  On  a  human  subject  these  investigations 
were  performed  in  one  case  by  Griffiths  (55),  and,  ac- 
cording to  Casper  (i6a),  in  one  case  by  Gueillot  and  in 
one  by  Bryson. 

Casper  (1.  c.)  makes  the  appropriate  statement  with  re- 
gard to  these  observations  that  the  cases  were  altogether 
obscured  by  existing  complications,  and  it  is  therefore  not 
possible  to  decide  which  histological  changes  were  due  to 
the  complication  and  which  were  due  to  the  influence  of 
castration.-  I  wish  to  call  attention  here  to  one  of  my 
observations  (esse  58),  in  which  a  castration  was  per- 
formed on  the  right  side  and  a  vasectomv  on  the  left  eight 


92 


days  before  death.  The  histological  investigation  gave 
here  also  no  clear  results,  because  in  the  histological  pic- 
ture everything  else  was  overshadowed  by  the  charac- 
teristic changes  of  the  so-called  "hypertrophy  of  the  pros- 
tate. The  histological  investigations  of  atrophic  prostates 
artificially  produced  by  castration  in  animals  are  also  not 
numerous,  but  give  results  which  agree  almost  com- 
pletely. It  was  proved  that  in  castrated  animals  the 
glandular  tissue  proper  atrophies  first,  and,  too,  very 
quickly.  Casper  (i6a),  to  whom  we  are  indebted  for  the 
thorough  descriptions  of  the  corresponding  investigations, 
writes  that  in  these  experiments  "the  changes  in  the 
glandular  part  of  the  prostate  amount  to  an  entire  destruc- 
tion." (I.e. p.  584).  The  atrophy  of  the  glandular  ducts 
after  castration  was  more  pronounced  in  rabbits  than  in 
dogs,  according  to  the  experiments  of  Casper;  this  pe- 
culiar difference  deserves  especially  to  be  mentioned.  It 
is  proved  that  genuine  myomata  as  well  as  genuine  ade- 
nomata may  occur  in  the  prostate ;  these  two  kinds  of 
tumors  have,  according  to  my  opinion,  nothing  to  do  with 
the  so-called  "hypertrophy"  of  the  prostate.  In  the  "path- 
ological-anatomical Institute  of  Krakau"  a  preparation  of 
a  genuine  myoma  and  of  a  genuine  adenoma  of  the  pros- 
tate is  preserved;  the  latter  possesses  all  the  character- 
istics of  a  malignant  growth  ("adenoma  destruens")  ; 
other  similar  examples  could  neither  be  found  in  the  prep- 
arations of  high-grade  "hypertrophy"  of  the  prostates 
preserved  in  the  same  Institute  nor  in  the  statistics  of  dis- 
sections kept  since  1852.  I  myself  have  not  during  the 
last  three  school  years  dissected  a  single  similar  case  in  a 
material  of  1100-1200  bodies.  Among  the  observations 
used  as  a  basis  for  the  work  under  consideration  there  is, 
therefore,  not  a  single  analogous  case. 

Also,  according  to  the  literature  previously  collected, 
one  must  assume  that  bv  "hypertrophy"  is  meant  the 
"mixed"  form  of  prostatic  hypertrophy,  that  is,  the  one 
which  is  formed  by  a  uniform  participation  of  the  glandu- 
lar tissue  proper  and  of  the  fibromusculostroma.  That 
there  really  does  not  exist  a  "pure"  form  of  "prostatic 
hvpertrophv"  was  unmistakably  shown  by  one  of  the 
most  prominent  investigators  in  this  domain,  Socin. 

In  my  investigation  before  becoming  acquainted  with 
tlie  literature  I  came  to  the  conviction    that    the    histo- 


93 


logical  pictures  of  the  "hypertrophy"  observed  in  my 
cases  could  be  arranged  naturally  in  a  coherent  line  of 
different  degrees  of  one  and  the  same  process.  Should  I 
press  the  mode  observed  by  myself  into  the  extensive 
pattern  of  to-day,  then  I  would  have  to  say  that,  without 
exception,  in  every  case  of  "prostate  hypertrophy"  investi- 
gated by  myself  the  "mixed"  form  could  be  demonstrated, 
and  that  the  enlarged  prostates  were  in  the  main  com- 
posed of  glandular  tissue  proper.  Later  on  it  will  be 
proved  how  forced  such  a  definition  would  be.  Not  only 
in  one  and  the  same  prostate,  but  alsO'  in  the  vicinity  of 
one  and  the  same  microscopical  section,  I  frequently 
found  all  the  forms  of  structural  changes  with  their  tran- 
sitional pictures.  They  are  therefore  in  no  way  to  be 
differentiated  from  each  other.  Moreover,  my  investiga- 
tion cannot  be  brought  into  conformiy  with  the  well- 
known  differentiation  of  a  diffuse,  focal  or  nodular  sub- 
class. This  differentiation  would  by  all  means  be  justi- 
fied, to  a  certain  extent,  according  to  the  macroscopical 
view  of  the  preparation,  but  under  the  microscope  there 
exists  no  difference  of  any  account  between  the  two  sub- 
classes. As  the  histological  changes  observed  by  myself 
of  the  hypertrophic  prostates  deviate  to  a  certain  extent 
from  those  of  the  manuals.  I  have  gone  into  detail 
with  regard  to  my  investigations.  The  character 
of  the  changes  which  take  part  in  the  "hypertrophic 
prostate"  will  be  best  understood  by  a  separate  representa- 
tion of  the  changes  observed  in  its  structural  component 
parts,  taken  singly,  i.  e.,  the  changes  observed  in  the 
glands,  in  the  muscle  fihrUlce,  and  in  the  connectiz'e-fisstte 
framezvork.  The  changes  in  these  three  component  parts 
•were  in  every  one  of  my  cases  zvithout  any  exception  in- 
variably alike;  the  existing  differences  betzveen  this  or 
that  case  consisted  in  the  main  only  in  a  different  locali- 
zation of  these  otherzvise  identical  processes.  Most  con- 
spicuous of  all  is  the  enlargement,  in  all  cases,  constantly 
observed,  of  'the  glandular  lumen  in  the  glandular  tissue 
proper ;  this  enlargement  appears  by  no  means  uniformly 
in  all  parts  of  the  enlarged  prostate  gland,  but  is  found 
only  here  and  there,  and  reaches  a  high  grade  at  one 
place  and  is  only  indicated  at  another.  In  the  lumen  of 
the  enlarged  glandular  ducts  there  is  nearly  constantly  a 
pathological  contents  present,  which  is  mainly  composed 

94 


of  desquamated  epithelial  cells,  occurring  either  singly  or 
in  rows.  These  desquamated  cells  are  most  frequently  of 
a  polygonal  or  of  a  cuboidal  form,  therefore  visibly  flatter 
than  the  normal  lining  of  the  glands  of  the  prostate.  Very 
frequently  retrograde  changes  are  to  be  observed, 
since  their  nuclei  do  not  stain  any  longer  with  the 
basic  dyes  or  become  only  pale  and  hazy;  the  death 
of  the  cells  is  also  proved  by  the  behavior  of  the 
cell-plasma,  which  loses  its  normal  appearance  and  ap- 
pears either  entirely  homogeneous  or  separated  into  ir- 
regular lumps  of  different  sizes.  In  other  still  more 
largely  altered  cells  the  cell  online  is  indistinct,  hazy  or 
uneven  as  mentioned.  Finally,  the  entire  collection  of 
enucleated  cells  is  changed  into  a  heap  of  irregular, 
equally  colored  lumps  and  grains  of  plasma.  They  are 
scattered  irregularly  in  the  lumen  of  the  enlarged  glandu- 
lar ducts,  found  now  alone,  now  in  little  heaps.  In  very 
many  glandular  ducts  such  cell  remains  quite  dead ;  cells 
form  into  homogeneous,  often  concentrical,  layers,  or 
they  form  into  a  mass  impregnated  with  lime-salts.  One 
can  then  meet  the  so-called  amyloid  bodies  in  their  differ- 
ent states  of  development. 

But  sometimes  no  amyloid  bodies  will  be  formed  from 
such  desquamated  cells  and  cell  remains.  In  the  lumen  of 
some  dilated  glandular  ducts  only  a  single  lump  is  found, 
to  fill  it  entirely  or  almost  entirely  and  consists  of 
an  amorphous,  homogeneous  or  finely  granulated 
mass.  Such  amorphous,  homogeneous  masses  seem 
to  be  related  to  the  genuine  amyloid  bodies,  because 
similar  but  small  amorphous  lumps  are  met  with  in  the 
other  glandular  acini,  aside  from  the  desquamated 
epithelium  and  genuine  amyloid  bodies.  Between  such 
amorphous  lumps  and  the  homogeneous  or  finely  granu- 
lated concretions  often  lying  beside  it,  which  remind  one 
by  their  polygonal  form  and  blunt  edges  of  the  non- 
striated,  non-calcified  amyloid  bodies,  there  exists  only 
an  insignificant  difference.  Finally,  it  is  easy  to  find  such 
places  in  which,  in  the  interior  of  the  homogeneous  mass, 
there  are  enclosed  here  and  there  either  smaller  or  greater, 
mostly  non-calcified  but  clearly  striated,  amyloid  bodies; 
then  we  shall  find  cell  remains  characterized  by  chromatic 
lumps,  and  then  more  or  less  changed  sometimes,  through 
apparently  normal  but  desquamated  epithelial  cells. 

95 


These  different  sub-classes  of  a  pathological  contents 
composed  mainly  of  desquamated  and  dying  epithelial 
cells — cell  remains,  loose  plasma  lumps  and  the  homo- 
geneous masses  probably  formed  by  these — will  be  cpn- 
stanly  found  in  the  enlarged  glandular  acini  of  every  en- 
larged prostate  gland.  As  this  picture  repeated  itself 
throughout  my  entire  observation  in  manifold  combina- 
tions, I  believe  it  is  not  necessary  to  cite  the  individual 
cases.  Besides  the  component  parts  already  mentioned 
of  the  pathological  contents  of  the  glands  there  is  some- 
times still  another  to  be  found.  This  other  is  the  leuco- 
cyte, which  is  easy  to  be  differentiated  by  its  characteristic 
polymorphous  nucleus  from  the  other  kind  of  cells. 
These  polynuclear  leucocytes  make  up  only  a  fraction  of 
the  pathological,  glandular  contents.  They  are  mostly 
found  at  scattered  places  of  the  proparation  without  any 
regularity.  Much  more  rarely  it  occurs  that  the 
contents  of  the  enlarged  glandular  acini  consists  ex- 
clusively of  leucocytes  and  has  the  characteristics  of  a 
genuine  suppurating  exudate.  Between  the  amount  of  the 
leucocytes,  to  a  greater  or  less  extent  in  the  enlarged  pros- 
tate gland  of  cases  i,  5,  14  and  60.  Much  more  rarely 
it  occurs  that  the  contents  of  the  enlarged  glandular  acini 
consists  exclusively  of  leucocytes  and  has  the  character- 
istics of  a  genuine  suppurating  exudate,  as  was  observed, 
for  instance,  in  case  15.  Between  the  amount  of  the 
leucocyte-containing  glandular  acini  and  the  proportion 
of  the  leucocytes  to  the  remaining  contents  there  seems  to 
exist  a  relation.  The  nearer  the  pathological  glandular 
contents  stand  in  a  morphological  respect  to  a  genuine 
suppurating  exudate,  the  more  numerous  are  the  en- 
larged glandular  acini,  which,  as  a  rule,  are  filled  with 
such  leucocyte-containing  masses. 

If  on  account  of  the  morphological  characteristics,  one 
should  call  this  process  a  suppurating  glandular  inflam- 
mation, then  we  might  say  that  the  intensity  of  the  sup- 
puration runs  parallel,  to  a  certain  extent,  with  its  de- 
velopment. I  have  already  mentioned  that  the  glandular 
lumen  is  for  the  most  part  entirely  and  densely  filled  with 
the  pathological  masses,  and  that  the  corresponding 
glandular  acini  are  in  most  cases  dilated.  I  never  had  the 
opportunity  to  observe  dilated  but  empty  glandular  acini. 
On  the  contrary,  these  acini  were  on«ly  dilated  when  there 

96 


was  present  in  their  lumen  an  increased  mass  of  epithelial 
cells,  mostly  pathological,  and  in  the  mildest  cases  des- 
quamated and  pretty  well  preserved.     A  contents  of  the 
composition    last    mentioned   occurs   by   no  means   fre- 
quently.      As  I  have  stated  before,  the  cells  contained  in 
the  mass  are  mostly  changed  pathologically.     As  long  as 
the  glandular  lumen  is  not  entirely  filled  with  this  mass 
the  normal  form  of  the  gland  is  preserved,  because  the 
compound  tubular  form  characteristic  of  the  normal  gland 
suffers  no  extensive  changes.     As  soon  as  the  mass  be- 
comes more  extensive  and  begins  to  fill  out  the  glandu- 
lar  lumen,    then   the   characteristic   glandular     structure 
is    gradually    lost.     The    walls    of    the    glandular    trbuli 
move    always    more    and    more    apart ;    the    intervening 
walls     which    limit    the    ramification    become    gradually 
thinner    and    flatter     (shorter),    until    they    are    trans- 
formed into  a  kind  of  a  ridge,  which  projects  from  the 
wall   into    the   lumen.     These    ridges   become   gradually 
flatter  in  the  more  strongly  dilated  acini.     Finally  they 
are  no  longer  visible  ;  and  the  corresponding  glandular 
part,  but  especially  the  ramification  of  the  tubules  with 
their  lateral  and  terminal  dome-shaped  outlets,  assume  the 
form  of  roundish  microscopical  cysts.     The  more  the  in- 
dividual glandular  acini  are  dilated  by    the    pathological 
contents,  and  the  more  numerous  the  terminal  branches  of 
a  single  glandular  system  that  suffer  a  dilation,  the  more 
pronounced  will  be  the  cystic  changes  in  the    glandular 
acini.   After  all  the  interlining  walls  of  the  enlarged  tubuli 
become  gradually  thinned  out  until  thev  disappear  com- 
pletely.    By  this  means  there  may  result  a  formation  of 
greater,   macroscopically    visible    cysts,     whereby    many 
enlarged    prostates,    especially    the    so-called    "diffuse" 
form,  take  on  in  section  the  well-known  spongy  appear- 
ance with  an   extremely  fine  outlme.     It  can  hardly  be 
doubted  that  if  this  process  has  lasted  a  suflicientlv  long 
time   and    is    always    progressing,    there    will    finally   be 
formed  greater  macroscopical  cysts.     Probably  this  will 
occur  easily  if  the  glands  suffer  from  the  supouratinaf  in- 
flammation already  mentioned,  as  under  such  conditions 
the  pathological  contents  of  the  gland  increase  rapidly. 

The  supposition  that  the  suppurating  process  in  a 
glandular  part  mav,  under  certain  conditions,  produce  the 
origin  of  proportionally  large  cysts,  becomes  verv  likely 

9.7 


by  reason  of  the  fact  that  the  cysts  observed  in  my  cases 
were  constantly  filled  with  pure  pus,  or  at  least  with  a 
contents  holding  many  leucocytes. 

To  complete  the  picture  of  the  changes  in  the  gland  of 
the  "hypertrophic"  prostate,  I  must  describe  the  behavior 
of  the  epithelium  lining  the  glandular  acini,  as  far  as  this 
epithelium  is  preserved. 

One  can  often  observe  that  the  wall  of  the  dilated  acini 
is  here  and  there  deprived  of  its  epithelial  lining. 
Rarely  it  is  missing  to  a  greater  extent,  and  then 
mainly  in  the  highest  degrees  of  dilatation  in  the 
cystically  changed  acini  and  especially  when  to  the 
mass  in  the  glands  a  relatively  great  quantity  of  leuco- 
cyes  is  added.  For  the  most  part  the  epithelial  lining  is 
missing  in  small  portions  of  the  wall ;  one  can  often  ob- 
serve the  bits  of  clesauamated  epithelium  cast  off  in  a  con- 
tinuous row  and  lying  near  its  place  of  origin. 
Som_etimes  it  approaches  in  such  a  connected  layer 
the  middle  of  the  glandular  lumen,  but  mostly  only 
individual,  usually  dying,  loose  cells  or  their  remains 
are  present  in  the  neighborhood  of  the  uncovered  wall. 
But  as  well  the  epithelium  becomes  altered  at  places 
where  it  is  not  missing.  The  more  the  gland  becomes  di- 
lated, the  flatter  will  be  the  epithelium.  From  the  cylin- 
dric  it  is  changed  to  a  cuboidal  form  and  finally  becomes 
flat.  At  this  stage  of  the  changes,  which  coincides  mostly 
with  a  very  high  degree  of  glandular  enlargement,  the 
normal  structure  of  the  epithelial  lining  becomes  gradu- 
ally lost,  as  the  compensating  cells  push  themselves 
through  little  by  little  between  the  flattened-out  and 
pushed-apart  cells  of  the  superficial  layer.  These  com- 
pensating cells  are  called  by  those  who  assume  the  pros- 
tate epithelium  to  be  a  double  layer — "the  deeper  layer." 
By  this  means  these  cells  are  forced  into  the  epithelial 
layer  proper,  and  disappear  gradually.  In  such  cases  the 
existence  of  those  compensating  cell  layers  can  only  be 
demonstrated  at  individual  places  in  the  wall. 

If  finally  the  dilatation  of  the  grandular  acini  has 
reached  the  highest  degree,  the  epithelium  becomes  a 
scale-like  thin  membrane,  in  which  here  and  there  only 
flat  nuclei  are  to  be  found.  These  are  at  last  entirelv  de- 
stroyed, so  that  the  pathological  conten'-'=  of  ^he  gfland 
com.es  to  lie  apparently  loose  in  a  space  within  the  stroma. 

98 


The  origin  of  such  a  space  situated  within  the  stroma  is 
the  harder  to  recognize,  since  the  prostate  gland,  as  is 
known,  has  no  "membrana    propria."     The    histological 
facts  regarding  the  "hypertrophic"  prostate  cited  above 
demonstrate  that  the  glandular  acini  suffer  a  passive  dila- 
tation through  the  accumulation  of  a  physiological  secre- 
tion, or,  what  occurs  more  frequently,  of  a  pathological 
contents  which  has  sometimes  indisputable  characteristics 
of  an  inflammatory  exudate.    In  this  regard  I  am  entirely 
in  accord  with  the  views  of  Socin   (119,  p.  39)  :     "Still 
more  one  gets  the  impression  of  a  passive  enlargement 
and  dilatation  of  the  normal  glandular  tubuli     *     *     *," 
with  the  only  difference  that  I  do  not  consider  the  dilated 
glands  in  the  majority  of  cases  as  normal.    The  frequent 
occurrence  of  desquamated  epithelial  cells  in  the  contents 
of  the  dilated  glandular  acini  seems  to  speak  very  defi- 
nitely for  the  proposition  that  the  secretory  processes  in 
the   prostate  glands   do  not   functionate  normally.     We 
must  assume  an  increased  and  a  vigorous  proliferation 
of  the  epithelium,  whereby  the  loss  caused  by  the  desqua- 
mation of  the  epithelial  cells  is  compensated.    We  have  to 
deal  here  with  a  process  very  similar  to  a  catarrh  of  the 
mucous  membrane.     I  could  never  observe  the  changes  in 
the  epithelium  which  might  be  taken  as  a  neoplasmatic 
proliferation.     By  other  authors  two  kinds  of  prolifera- 
tion in  this  sense  were  described.    One  should,  apparently, 
depend  upon  the  fact  that  the  epithelium  becomes  strati- 
fied, whereby  the  superficial  cells  which  are  lying  opposite 
the  center  of  the  glandular  lumen  lose  their  nuclei  and 
become  more  polygonal  and  big-ger  than  the  peripheral 
cells.     The   other   kind   of  changes   depend,   apparently, 
upon  a  sprouting  of  new,  partly  solid,  partly  hollow  cell 
plugs,   from  which   later  on  new  glandular  tubules  are 
formed.     In  spite  of  very  careful  researches,  neither  the 
one  nor  the  other  kind  of  this  proliferation  could  I  find 
in  the  enlarged  prostate  glands  e:^amined  by  me,  provided 
that  the  preparation  was  cut  correspondingly  thin   (not 
above  0.01  =  104  thickness).     On  the   other  hand,  it  is 
not  hard  to  find  such  pictures  as  are  described  by  Birch- 
Hirschfeld  and  Jores  in  thicker  preparations,  in  which  a 
few  layers   of   cells   were  arranged    above    each    other. 
Jores  constantly  observed  a  lumen  in  the  cell  plugs  that 
were  apparently  solid.      In   the  thinner  preparation   it  is 

99 


easy  to  convince  onself  that  these  lumina  are  just  as  wide 
as  those  of  the  normal  glandular  tubuli,  and  that  they 
are  constantly  lined  with  a  normal,  single  layer  of  high, 
cylindrical  epithelium.  In  the  serial  sections  one  can, 
furthermore,  easily  observe  that  in  the  following  section 
this  lumen  apparently  becomes  narrower,  and  that  the 
epithelium  apparently  comes  stratified.  These  pictures 
have  their  origin  in  this  fact,  that  the  following  cuts 
always  include  more  of  the  tubular  wall,  so  that  a  few 
layers  of  cells  fall  within  the  section.  Also  in  the  trans- 
verse section  of  the  tubuli  a  similar  state  of  afifairs  is  to 
be  observed,  provided  the  preparation  be  sufficiently 
thick.  The  apparent  striation  of  the  epithelium  is  pro- 
duced by  the  wave-like  course  of  the  prostatic  glandular 
tubuli.  For  this  reason  they  are  very  rarely  cut  exactly 
transversely.  By  using  the  corresponding  thin  section 
one  can  easily  convince  himself  that  that  which  was  looked 
upon  as  a  new-formed  glandular  tubule  by  Birch-Hirsch- 
feld  and  Jores  was  nothing  but  an  altogether  normal 
glandular  branch,  which  was  not  yet  enlarged  by  the 
accumulated  pathological  contents.  By  similar  technical 
mistakes  the  incorrect  conclusion  of  the  French  investi- 
gators is  to  be  explained,  only  with  the  difference  that 
here  the  faulty  observation  was  referred  to  the  enlarged 
glandular  acini.  If  such  a  glandular  acinus  be  opened 
by  a  cut  at  its  greatest  diameter  or  near  it,  then  its  pe- 
ripheral epithelial  lining  will  be  divided  longitudinally, 
i.  e.,  vertically,  and  will  appear  in  its  real  form,  i.  e.,  as  a 
single  layer.  But  the  case  will  be  entirely  different  if 
the  cut  open  a  cystically  enlarged  gland  near  its  wall 
parallel  with  and  near  a  tangent  surface.  The  part  of 
the  glandular  wall  divided  by  this  forms  a  very  shallow, 
dome-shaped  sphere  or  cylindrical  section.  Then  it  may 
easily  occur  that  the  cut  may  not  at  all  reach  the  lumen 
of  the  gland,  but  may  «ink  itself  in  its  whole  extent  in 
the  epithelial  lining.  But  the  peripheral  epithelial  cells 
are  cut  through  at  different  heights  :  the  ones  lying  in  the 
middle  are  cut  near  the  summit ;  the  others  lying  nearer 
the  periphery  are  cut  near  the  base,  that  is,  the  part  which 
contains  the  nucleus.  For  this  reason  we  find  that  the 
cells  lying  in  the  middle  of  the  corresponding  section  of 
the  glandular  wall  have  no  nuclei,  while  those -at  the  pe- 
riphery have,  and  the  whole  makes  the  impression  of  a 


glandular  acinus  filled  with  the  proliferating  cells  of  the 
stirated  epithelium.  That  this  is  so  is  demonstrated  by 
the  difference  in  size  between  the  peripheral  and  the  cen- 
tral cells,  as  mentioned  by  the  French  investigators,  which 
difference  is  only  apparent. 

The  changes  in  the  glandular  tissue  proper  already  de- 
scribed are,  as  has  been  mentioned,  very  irregularly  dis- 
tributed in  the  enlarged  prostate  gland :  one  can  observe 
in  one  and  the  same  preparation,  besides  the  high-grade 
and  differently  changed  parts  of  the  gland,  also  entirely 
normal  parts.  The  variety  of  combinations  caused  by  this 
irregular  distribution  of  changes  is  so  great  that  it  seems 
impossible  to  enumerate  them  all.  In  this  respect  there 
is  no  regularity,  except  that  each  individual  group  of 
similarly  changed  glandular  acini  belongs  to  one  and  the 
same  main  duct.  The  changes  localized  in  a  glandular 
system  do  by  no  means  constantly  occupy  the  whole  ex- 
tent of  such  duct ;  on  the  contrary,  it  may  often  be  ob- 
served that  certain  parts  of  a  glandular  system  gi-p-  now 
greatly  changed,  now  only  a  little  or  not  at  all.  We  see 
here  a  row  of  transitional  pictures.  The  highest  grades 
of  the  changes  are  generally  to  be  observed  in  those  enu- 
cleatable,  in  some  enlarged  prostate  glands  even  macro- 
scopical  nodules.  These  nodules  are  called,  as  is  known, 
by  a  variety  of  names,  as,  for  instance,  "Fibromyoma," 
"Adeno-mvoma  Adenoma,"  &c.,  &c. 

From  the  foregoing  representation  it  will  be  seen  that 
we  cannot  speak  of  a  genuine  neoplasmatic  proliferation 
of  the  glandular  tissue  proper  of  the  enlarged  prostate 
glands  ;  and,  as  the  majority  of  these  well-defined  nod- 
ules that  can  be  enucleated  consist  exclusively  of  the 
much  dilated  glandular  acini,  I  gave  to  these  nodules, 
without  seaiching  for  other  names,  the  name  of  "pseiido- 
adenoma."  The  number  of  the  changed  glandular  acini 
is,  in  certain  cases  of  prostatic  enlargement,  very  varying, 
but  in  general  it  can  be  said  that  the  number  is  greater 
the  higher  the  grade  which  the  enlargement  of  the  pros- 
tate as  a  whole  reaches. 

At  first  glance  it  seems  as  if  the  number  of  the  glands 
in  the  enlarged  prostate — that  is,  the  amount  of  glandular 
tissue  proper — were  absolutelv  increased  in  proportion  to 
the  normal  condition.  Sometimes  it  is  by  no  means  easy 
to  avoifl  this  impression,  especially  if  one  encounters  the 


dilated  glandular  acini  in  places  of  the  preparation  where 
normally  they  are  less  numerous  and  where  generally  only 
a  few  excretory  ducts  with  short  dilatations  lie  in  an 
abundant  stroma,  as  is  the  case  especially  in  the  central 
parts  of  the  prostate  in  the  neighborhood  of  the  urethra. 
By  an  investigation  of  my  cases,  made  as  exact  as  pos- 
sible, I  was  convinced  that  in  no  one  of  them  is  the 
glandular  tissue  absolutely  increased.  The  increase  of 
the  glandular  tissue  is  only  apparent,  and  arises  wholly 
through  the  dilatation  of  the  lumen. 

The  circumstance  that  we  frequently  encounter  the 
glandular  tissue  of  the  enlarged  prostate  gland  in  the 
form  of  "pseudo-adenoma"  at  uncommon  places  in  the 
close  vicinity  of  the  urethra  depends,  as  I  shall  later  dem- 
onstrate, upon  a  displacement  and  a  storing  up  respec- 
tively of  a  ''pseudo-adenoma"  that  is  already  formed  and 
is  still  growing. 

It  is  known  that  the  enlargement  of  the  so-called  an- 
terior commissure  is  a  very  rare  occurrence.  Aside  from 
the  cases  cited  by  Klebs  (305,  p.  1123  R),  Quain's  (108), 
and  the  three  observations  mentioned  in  Thompson's 
statistics,  I  found  in  the  literature  within  my  reach  only 
three  other  cases.  These  last  cases  were  published  by 
Sahlange  (123).  From  anatomical  investigations,  espe- 
cially the  one  of  Aschoff  (2),  it  may  be  seen  that  in  the 
majority  of  cases  only  a  few  small  and  but  little  ramified 
gland  tubules  are  present  in  the  vicinity  of  the  anterior 
prostatic  commissure;  that  sometimes  none  exist  at  this 
place,  and  that  only  exceptionally  abundant  glandular 
tissue  is  present,  which  then  forms  a  kind  of  anterior  lobe 
of  the  prostate,  and  which  exceptionally  may  be  placed 
below  as  far  as  the  dorsal  side  of  the  cavernous  urethra 
(Luschka  [75]).  The  fact  that  the  enlargement  of  the 
anterior  prostatic  commissure  occurs  very  rarely  corre- 
sponds entirely  with  my  investigation.  If  in  the  so- 
called  "hypertrophy"  of  the  prostate  the  genuine  new 
formation  and  the  increase  of  the  gland  tubules  play  a 
main  role,  then  the  enlargement  of  the  anterior  prostatic 
commissure  should  occur  much  more  frequently. 

The  gland  groups  lying  in  front  of  the  urethra  do  not 
differ  with  regard  to  their  origin  nor  with  regard  to  their 
structure  from  other  gland  tubules  of  the  prostate.  Gen- 
erally they  have  too  small  dimensions  and  are  not  nu- 


merous  enough  to  produce  by  their  dilatation  changes 
which  can  be  recognized  macroscopically.  In  those  ex- 
ceptional cases,  on  the  other  hand,  in  which  at  the  anterior 
commissure  there  are  more  numerous  and  more  richly 
branched  gland  collections,  their  dilatation  is  capable  of 
producing  a  macroscopic  and  even  a  high-grade  enlarge- 
ment of  the  anterior  commissure. 

One  can  raise  objection  that  it  is  altogether  inconceiv- 
able that  the  dilatation  of  the  glandular  acini  alone  should 
be  capable  of  producing  such  an  extensive  enlargement  of 
the  entire  prostate  gland  as  is  sometimes  observed.  To 
this  I  must  reply  that  pronounced  extensive  enlargements 
of  the  prostate  occur  only  exceptionally,  and  that  in  the 
majority  of  cases  the  enlargement  of  the  prostate  does  not 
exceed  a  mild  degree ;  furthermore,  that  even  the  greatest 
cases  of  hypertrophy  of  the  prostate  up  to  the  present  time 
published  do  not  exceed  the  size  of  an  apple,  while  gen- 
uine neoplasmata,  as  for  instance  the  wrongly  included 
uterus  myomata,  are  not  restricted  in  their  growth. 
Finally,  we  have  to  consider  that,  even  if  the  glandular 
dilatation  plays  here  a  main  role,  one  can  hardly  maintain 
that  this  dilatation  is  the  only  cause  of  enlargement  of 
the  prostate.  This  holds  good  only  for  the  beginning 
stages. 

That  the  passive  dilatation  of  the  glandular  acini  alone 
is  able  to  cause  a  considerable  enlargement  of  the  entire 
prostate  gland  is  nothing  remarkabte.  Long  before  all 
the  glandular  acini  suffer  from  the  changes  previously 
mentioned  the  prostate  gland  may  reach  very  great 
dimensions  and  still  steadily  grow  larger.  A  similar 
process  occurs  in  all  retention  cysts  which  enlarge,  as 
long  as  the  epithelial  lining  is  so  far  preserved  as  to  be 
still  capable  of  secreting."  To  select  an  example  in  which 
we  cannot  as  a  rule  speak  of  an  active  proliferative 
process,  hydromphrosis  mav  here  be  mentioned,  which 
enlargernent  ceases  only  with  the  final  atrophy  of  the 
renal  epithelium;  but  before  this  occurs  the  organ  may 
reach  the  size  of  a  man's  head. 

If  one  wishes  to  find  out  exactly  the  role  which  the 


'In  the  prostate  the  dilatation  of  the  acini  may  even  pro- 
gress after  the  loss  of  the  epithelium,  if  the  additional  accumu- 
lation of  the  secretions  in  a  given  case  be  caused  by  suppura- 
tion. 


ro^ 


passive  enlargement  of  the  acini  plays  here,  it  is  not  suffi- 
cient to  examine  several  or  more  preparations  of  any  part 
of  the  prostate  gland,  but  one  must  carefully  go  over  the 
preparations  of  the  main  parts  and  of  every  one  of  the 
main  planes/ 

The  passive  dilatation  of  the  glandular  acini  is  un- 
doubtedly a  consequence  of  pathological  processes  taking 
place  within  them,  whereby  a  great  accumulation  of  their 
contents  is  produced.  The  cause  of  the  obstruction  is 
referred  to  the  presence  of  the  amyloid  bodies. 

It  is  easy  to  demonstrate  the  real  and  primary  causes 
of  the  passive  glandular  dilatation  in  the  changes  localized 
in  the  stroma.  In  all  the  cases  of  "hypertrophy  of  the 
prostate"  examined  by  myself  I  met,  ivithout  exception, 
with  such  changes  in  the  vicinity  of  the  stroma  as  were 
able  to  clear  up  all  the  phenomena.  These  changes  de- 
pend upon  a  proliferative  coniiective-tissue  process. 

As  the  first  stage  of  these  processes,  may  be  designated 
the  appearance  of  infiltrations,  which  consist  of  small, 
round  cells  poor  in  protoplasm,  with  dark-colored  nuclei, 
and  similar  to  granulation  tissue.  I  shall  leave  it  unde- 
cided where  these  infiltrations  take  their  origins,  whether 
they  generate  from  the  fixed  con.-tis.  elements  or  from 
lymphocytes,  which,  however,  are  regarded  by  Ribbert 
as  a  special  kind  of  cell.  (Comp.  "Das  Patholojische 
Wachstum  der  Gervebe.  Bonn,  1896.)  As  a  matter  of 
fact,  such  infiltrations  appear  mainly  in  organs  suffering 
from  a  chronic,  productive  process,  and  it  is  demonstrated 
indisputably  that  genuine  con.-tis.  is  found  to  replace 
these  infiltrates  in  the  more  advanced  stages,  and  this 
con.-tis.  becomes  finally  cicatricial  tissue,  poor  in  vessels, 
firm  and  compact.  The  small-cell  infiltrates  observed  by 
myself  in  the  enlarged  prostate  gland  are  of  different  ex- 
tent and  are  varying  in  density,  now  small,  now  large, 
now  compact  and  now  very  loose. 

There  is  apparently  no  regularity  to  be  noted  in  their 
localization,  except  that  for  the  greater  part  they  have 
their  seat  just  beneath  the  gland  epithelium  or  quite  close 
to  it.. 


"It  is  essentially  necessary  to  examine  the  entire  horizontal 
section  of  the  whole  prostate  gland  to  obtain  certain  land- 
marks, for  which  a  magnifying  glass  (Preparation  microscope) 
and   the  weakecst  objectives  are   well  adapted. 


104 


Sometimes,  however,  these  infiltrations  appear  loose  in 
the  stroma  far  away  from  the  glandular  wall,  but  they  are 
rather  rare,  and  there  are  constantly  beside  them  nu- 
merous subepithelial  infiltrations.  The  latter  appear,  as 
a  rule,  in  groups  irregularly  scattered  in  the  different 
parts  of  the  prostate  gland ;  they  are  most  frequently  met 
with  in  the  zone  of  the  prostate  gland,  which  is  equally 
distant  from  the  superficial  capsule  and  from  the  urethra. 
Less  often  they  are  found  in  the  central  parts  of  the  pros- 
tate related  to  the  urethra,  beneath  the  epithelium  of  the 
main  excretory  ducts.  Neither  are  they  missing  in  the 
most  peripheral  parts  lying  very  near  the  capsule,  where 
they  also  attach  themselves  to  the  wall  of  the  terminal 
branches  of  the  glands.  Such  infiltrates  lying  quite  in  the 
periphery  occur  rather  rarely  in  the  enlarged  prostate 
gland  and  do^  not  reach  any  large  size. 

Aside  from  these  infiltrates,  there  are  found  in  the  pros- 
tate gland,  beneath  the  epithelium  of  the  gland  tubules, 
older  groups  of  con.-tis.  composed  of  spindle-shaped  cells 
with  elongated  nuclei,  which  groups  here  and  there  begin 
to  assume  the  characteristics  of  fibrous  con.-tis.  By  such 
con.-tis.  groups  a  gland  tubule  or  a  group  of  tubules  is 
generally  surrounded.  The  tubuli  enclosed  in  such  con.-tis. 
groups  have  sometimes  a  narrow  lumen,  even  narrower 
than  normal.  Within  the  con.-tis.  group  itself  there  is 
generally  no  sign  of  muscular  cells  to  be  detected,  or  else 
we  see  only  a  very  few,  which  are  scattered  exclusively  in 
the  peripheral  parts  of  the  groups.  They  are  therefore 
either  destroyed  by  atrophy  or  they  are  displaced  outward 
by  the  connective-tissue  abundantly  formed  in  the  sub- 
epithelial stroma.  The  extent  of  such  a  con.-tis.  group  is 
very  varied.  Some  gland  tubuli  are  hardly  surrounded  by 
a  few  rows  of  con.-tis.  cells.  In  other  cases,  on  the  other 
hand,  the  latter  form  a  compact  mass  composed  of  nu- 
merous cell  layers,  by  which  the  intertubular  septa  ap- 
pear to  be  much  thickened.  This  thickening  of  the 
glandular  walls  is  also  capable  of  adding  to  the  enlarge- 
ment of  the  prostate  gland,  aside  from  the  passive  dilata- 
tion of  the  glandular  acini ;  but  it  is  by  no  means  so  pro- 
nounced and  extensive  as  to  gain  an  essential  impor- 
tance for  the  size  of  the  prostate :  it  plays  here,  in  my 
opinion,  a  relatively  subordinate  role. 

The  connective-tissue  groups  described   occur  also  in 


the  wall  of  even  highly  dilated  gland  acini ;  there  is  only 
a  part  of  the  glandular  wall  included  by  them,  as  they  do 
not  surround  the  glandular  acini  uniformly.  The  thick- 
ness of  the  connective-tissue  layers  is  in  such  a  place,  at 
any  rate,  very  variable ;  for  the  greater  part  they  consist, 
however,  of  at  most  two  to  three  cell  layers. 

These  con.-tis.  groups  appear  in  the  same  way  as  the 
infiltrates,  that  is,  in  groups  in  the  different  parts  of  the 
prostate.  They  are  more  easily  and  more  frequently  to 
be  found  in  the  parts  that  are  central  with  relation  to  the 
urethra  than  in  the  peripheral  parts.  In  the  latter  they 
are,  however,  much  more  rare  than  the  infiltrates.  In 
some  preparations  only  such  con.-tis.  groups  will  be 
found;  in  the  majority  of  cases,  on  the  other  hand,  there 
are  at  the  same  time  in  the  vicinity  of  the  same  section, 
aside  from  the  con.-tis.  groups,  numerous  small-cell  in- 
filtrates which  often  lie  next  to  these  con.-tis.  groups. 
The  extent  of  these  changes,  in  the  infiltrates  as  well  as  in 
the  con.-tis.  groups,  is  as  different  in  the  different  pros- 
tate glands  as  the  passive  gland  changes.  In  general 
there  exists  between  the  two  kinds  of  changes  a  certain 
parallelism,  though  this  is  by  no  means  constant. 

So  we  shall  find  in  a  prostate  gland  relatively  little 
change  in  the  stroma,  while  the  passive  gland  dilatation 
has  a  great  extent,  and  vice  versa. 

Of  frequent  occurrence  are  the  genuine  cicatrices  of 
the  enlarged  prostate  glands,  which  are  composed  of 
nearly  homogeneous,  weakly-staining  con.-tis.  groups 
poor  in  nuclei.  Within  such  cicatrices  there  is  often  found 
a  very  narrow  lumen  lined  with  epithelium. 

The  form  of  the  epithelial  cells  is  here  sometimes  still 
normal,  but  oftenest  they  are  flattened.  It  sometimes 
happens  that  the  flattened  cells  fuse  together  into  a  homo- 
geneous, glass-like  ring;  sometimes  this  is  no  more 
visible,  and  then  the  origin  of  the  very  narrow  lumen 
which  lies  loose  m  the  cicatricial  tissue  is  divined  with 
difficulty.  The  meaning  of  such  lumina  is  sometimes  ex- 
plained by  the  presence  of  amyloid  bodies.  In  the  vicinity 
of  such  groups  of  cicatrices  there  occurs  sometimes  in- 
sulas  of  new  con.-tis.  composed  of  spindle-shaped  cells, 
or  even  isle-like  small-cell  infiltrates.  The  former  as  well 
as  the  latter  lie  now  beneath  the  epithelium  of  the  atrophic 
glands,  now  somewhat  further,  with  the  cicatricial  pro- 

io6 


longations. 

These  cicatricial  groups  are  found,  however,  just  as  is 
the  group  of  new  con.-tis.,  mainly  in  the  central  portions 
of  the  prostate;  and  they  occur  isle-like  in  the  neighbor- 
hood of  the  gland  tubuli.  It  seems  hardly  necessary  to 
demonstrate  that  the  stroma  changes  described  are  noth- 
ing else  but  different  stages  of  development  of  a  pro- 
liferated con.-tis.  and  a  result  of  a  very  chronic  productive 
process.  They  appear,  as  a  rule,  in  the  form  of  sharply 
limited  groups  in  the  central  parts  of  the  prostate  glands, 
and  then  mostly  in  the  immediate  or  very  near  neighbor- 
hood of  the  gland  tubuli,  but  usually  just  beneath  the  epi- 
thelial lining.  Such  periglandular  changes  are  undoubt- 
edly capable  of  hindering  the  emptying  of  the  glandular 
contents,  provided  that  they  localize  themselves  in  the 
neighborhood  of  the  greater  excretory  ducts  of  the  pros- 
tate. The  small-cell  infiltrate  surrounding  a  small  ex- 
cretory duct  is  capable  even  alone  of  producing  a  certain 
narrowing  of  the  excretory  duct  and  with  it  an  obstruc- 
tion to  the  outflow  of  the  secretion  from  the  peripheral, 
glandular  parts.  The  dilatation  of  the  latter  will  be  the 
more  quickly  formed  the  more  abundant  the  contents  are, 
which  especially  happens  in  consequence  of  the  patho- 
logical epithelial  changes  already  described.  In  a  like 
manner  the  narrowing  of  the  excretory  duct  and  the 
blocking  of  the  secretion  is  produced  by  the  ring-like 
cicatrices  of  the  stroma,  which,  under  certain  conditions, 
may  produce  an  absolute  closure  of  the  gland  duct.  But 
it  may  also  come  to  a  genuine  obliteration  of  the  gland 
duct  if  the  epithelium  of  the  surrounding  glandular  septa 
(which  is  infiltrated  with  small  cells  and  thereby  pushed 
apart)  or  if  the  epithelium  of  the  excretory  duct  be  des- 
quamated. (Table  X,  Fig.  i8,  12,  u).  Then  the  sur- 
rounding, denuded,  small-cell  infiltrate  fuses  together  and 
fills  entirely  the  lumen  of  the  already  narrowed  excretory 
duct.  This  will  finally  be  entirely  obliterated  in  conse- 
quence of  the  transformation  of  the  infiltrate  into  cica- 
tricial tissue.  One  can  comparatively  often  observe  the 
most  varied  stages  of  obliteration. 

Even  if  it  should  happen  that  one  should  demonstrate 
that  in  some  cases  of  "prostatic  hj^pertrophy,"  contrary 
to  my  statements,  an  active  neoplasmatic  proliferation  of 
the  glandular  tissue  really  takes  places,  the  circumstance 


107 


that  the  smah-cell  infiltrates  sometimes  break  through  the 
glandular  wall  and  force  themselves  into  the  lumen  of  the 
gland  at  any  rate  would  not  be  without  importance.  By 
the  cells  of  such  an  infiltrate  not  only  the  individual  parts 
of  the  gland  ducts  are  separated  from  each  other,  but  the 
individual  epithelial  cells  are  also  pushed  apart,  which,  in 
the  opinion  of  Ribbert  (Das  Pathologische  Wachstum  der 
Gewebe.  Bonn,  1896),  might  be  a  cause  of  the  neoplas- 
matic  proliferation  and  growth  of  the  epithelium. 

The  great  importance  of  the  changes  of  the  stroma 
already  described  is  not  only  to  be  learned  from  their 
kind  and  localization,  but  also,  so  to  speak,  to  be  directly 
observed  from  the  following  representation.  In  some 
enlarged  prostate  glands  one  sees  wedge-shaped  sections 
composed  of  dilated  glandular  acini  and  lying  with  their 
bases  against  the  periphery  of  the  prostate,  and  at  the  cen- 
trally-pointed apices  we  find  an  excretory  duct,  narrowed 
by  a  ring-shaped,  small-cell  infiltrate,  or  by  a  ring- 
formed  cicatrix,  or  obliterated. 

The  relation  of  the  changes  in  the  con. -tis. -like  peri- 
glandular stroma  to  the  passive  dilatation  of  the  pe- 
ripheral, glandular  ramifications  is  not  at  all  doubtful  in 
such  pictures.  These  sometimes  include  a  very  great  part 
of  the  prostate  gland ;  the  new  infiltrate  or  the  obliterating 
cicatrix  lies  not  seldom  at  the  outlet  of  the  excretory  duct 
in  the  urethra. 

Thus  we  learn  to  understand  how  it  is  possible  that 
the  primarv  changes  of  the  stroma,  which  are  rela- 
tively unimportant  and  only  slightlv  extensive,  should 
have  such  great  consequences  and  should  be  capable  of 
producing  enlargement  of  the  prostate  gland.  The  patho- 
genetic importance  of  the  changes  in  the  stroma  lies 
mainly  in  its  localization.  The  dilatation  of  the  glandular 
acini  and  the  prostatic  enlargement  produced  through 
this  is  only  possible  when  the  changes  in  the  stroma  have 
their  seat  in  the  vicinity  of  the  excretorv  ducts  ;  and  it 
becomes  more  quickly  and  more  extensively  developed  the 
nearer  to  the  urethra  the  excretory  ducts  are  when  they 
become  narrowed  and  obliterated. 

In  some  cases,  especially  in  high-grade  prostate  en- 
largements, it  seems  impossible  to  demonstrate  DI- 
RECTLY the  causative  relations  between  the  changes  in 
the  stroma  and  those  in  the  glands  in  one  and  the  same 

1.08. 


preparation.  This  is  due  to  the  fact  that  the  gland-tubuli 
of  the  prostate  run  twisted,  whereby  the  individual  sec- 
tions never  come  to  lie  at  the  same  level. 

This  twisting  is  more  pronounced  in  older  individuals 
than  in  3'ounger  ones.  For  this  reason  the  cut  executed 
at  the  level  of  a  certain  gland  duct  is  never  able  to  divide 
it  parallel  with  its  axis  throughout  its  whole  length,  but 
it  opens  the  lumen  of  the  duct,  mostly  at  different  places, 
in  an  oblique  direction.  For  the  same  reason  the  histo- 
logical picture  of  the  prostate  gland  does  not  correspond 
to  the  schematic  representation  of  its  structure.  In  gen- 
eral the  excretory  ducts  of  the  prostate  gland  and  their 
tubular  ramifications  run  in  the  direction  of  the  radii  of  a 
half-sphere,  the  center  of  which  lies  somewhere  in  the 
neighborhood  of  the  colliculus  seminalis.  The  surfaces 
of  the  section  running  horizontally  (i.  e.,  vertically  tO'  the 
axis  of  the  urethra)  divide  those  glandular  systems 
throughout  their  whole  extent  whose  ramifications  lie  at 
the  level  of  the  colliculus  seminalis.  The  relation  of 
stroma  and  glandular  changes  in  one  and  the  same  prepa- 
ration can  therefore  only  be  demonstrated  in  sections  made 
at  the  level  of  the  colliculus  seminalis.  In  preparations 
made  from  sections  above  and  below  this,  this  relation 
can  only  be  demonstrated  by  serial  sections,  since  the 
changes,  as  before  mentioned,  are  extremely  irregularly 
distributed,  because  now  this  now  that  part  of  the  pros- 
tate gland  is  changed.  If,  therefore,  the  glandular  system 
which  branches  posteriorly  at  the  level  of  the  colliculus 
seminalis  accidentally  remained  normal,  then  only  will 
the  dififerent  kinds  of  stroma  changes  be  found,  aside 
from  the  glandular  dilatation,  in  one  and  the  same  prepara- 
tion ;  but  one  does  not  succeed  (aside  fro-m  the  senile  sec- 
tions) in  demonstrating  the  direct  relation  of  both  types 
of  the  changes  in  one  and  the  same  preparation.  In  the 
greater  and  also  in  the  milder  grades  of  enlargement  of 
the  prostate  there  are  still  other  processes  at  play  by  which 
the  picture  is  obscured.  It  is  the  deposit  of  certain  tissue 
sections  due  to  the  development  of  the  previously  men- 
tioned pseudo-adenomata,  by  which  in  certain  cases  it  be- 
comes impossible  to  find  the  excretory  ducts  belonging  to 
a  group  of  dilated  glands  and  to  recognize  where  the  cause 
of  the  glandular  dilatation  lies  to  which  the  stroma 
changes  are  respectively  to  be  referred.     This  shows  that 

109 


the  explanation  of  the  process  of  the  prostate  enlarge- 
ment becomes  impossible  without  the  investigation  of  the 
incipient  stages  of  this  process.  In  it,  in  my  opinion,  is 
to  be  sought  the  reason  why  the  views  of  the  different 
investigators  differ  so  much  with  regard  to  the  histo- 
genesis of  the  "hypertrophy"  of  the  prostate;  it  could  not 
be  otherwise  as  long  as  one  examined  only  the  advanced 
cases  in  which  the  original,  relatively  simple  conditions 
were  long  ago  eradicated. 

I  have  already  mentioned  that  the  "pseudo-adenomata" 
are  in  the  main  to  be  referred  to  the  passive  glandular 
changes.  The  observation  was  made  long  ago  that  these 
growths  consist  mainly  of  glandular  tissue.  They  are 
predominantly  composed  of  the  dilated  and  more  or  less 
cystically  changed  acini.  The  gland  septa  are  at  these 
places  mostly  very  thin,  and  contain  very  few  muscular 
elements.  On  the  other  hand,  there  occur  in  the  neigh- 
borhood of  the  pseudo-adenomata  places  in  which  the 
glandular  septa  are  thickened.  The  gland  tubuli  them- 
selves show  no  dilatation,  and  the  stroma  seems  to  be 
composed  of  closely  packed,  spindle-shaped  con".-tis.  cells. 
Such  places  were  wrongly  assumed  to  be  a  proof  of  a 
proliferation  of  the  muscle  elements  of  the  stroma ;  also 
the  spindle-shaped  con.-tis.  cells  were  wronglv  taken  for 
muscle  cells.  Many  years  ago  the  same  remark  was  made 
by  an  investigator  of  even  the  prominence  of  Rindfleisch, 
when  he  said :  "Most  authors  take  these  spindle-cells  for 
muscular,  and  therefore  designate  the  new  growth  as 
fiibro-muscular.  I  have  some  hesitation  in  accepting  this 
nomenclature  ..."  (311,  p.  581).  Possibly  the  view 
originated  in  thf^  fact  that  the  tumors  that  can  be  enu- 
cleated are  nothing  but  genuine  m\omata ;  by  the  usage 
of  the  faulty  lenses  employed  in  former  times  it  was  easy 
to  overlook  the  narrow  glandular  lumina  included  within 
the  soindle-cell  groups.  In  the  neighborhood  of  these 
spindle-cell  groups  I  could  never  demonstrate  a  greater 
accumulation  of  muscle  cells ;  on  the  contrarv,  such  groups 
are  always  verv  poor  in  muscular  elements;  sometimes 
these  are  entirely  missing. 

Furthermore  one  can  essih-  convince  oneself  on  serial 
sections  that,  aside  from  spindle-cell  groups,  there  are  also 
constantly  present  dilated  acini  in  the  pseudo-adenoma. 
The  pseudo-adenomata  observed  in  the  so-caJled  nodular 


form  of  the  hypertrophy  of  the  prostate  develop,  there- 
fore, from  processes  which  do  not  qualitatively  differ 
from  the  characteristic  conditions  of  the  so-called  "dif- 
fuse" form  of  hypertrophy  of  the  prostate.  The  macro- 
scopical  dift'erence  so  striking  between  these  two  forms 
proves  under  the  microscope  to  be  mainly  quantitative. 
I  have  mentioned  before  that  the  most  extensive  glandular 
dilatations  are  to  be  found  in  the  vicinity  of  the  pseudo- 
adenomata.  Besides,  the  difference  is  further  conditioned 
by  a  circumstance  which  gives  the  characeristic  macro- 
scopic appearance  to  the  pseudo-adenomata ;  it  is  that  the 
capsule  which  surrounds  the  pseudo-adenomata  consists 
of  concentric  layers  of  muscle  elements. 

By  the  examination  of  the  early  stages  of  the  process 
one  can  demonstrate  that  this  capsule  is  by  no  means  a 
new-formed  component  part  of  the  pseudo-adenomata, 
but  is  formed  from  already  present  none-proliferative  ele- 
ments. 

The  muscle  bundles  which  surround  the  glandular  rami- 
fications running  in  different  directions  are,  according  to 
the  increasing  glandular  dilatation,  gradually  pushed  out- 
side, together  with  the  walls  of  the  acini,  and  arrange 
themselves  in  concentric  rows  around  the  cystically 
dilated,  empty  spaces.  If  at  the  same  time  a  larger  group 
of  glands  which  terminate  in  a  common  excretory  duct 
suffers  a  dilatation,  then  gradually  there  will  be  formed 
at  the  periphery  of  the  gland  group,  which  assumes  a 
more  and  more  sphere-like  form,  a  concentric  muscle 
ring,  which,  together  with  the  connective-tissue  elements, 
becomes  a  kind  of  capsule. 

In  consequence  of  its  composition,  the  capsule  thus 
formed  is  elastic  and  exerts  a  certain  counter-pressure 
on  the  accumulated  contents  in  the  dilated  acini ;  for  this 
reason  the  capsule  retroacts  on  section  and  the  contents 
swell  out.  But  if  the  capsule  remain  intact  during  sec- 
tion of  the  prostate,  then  the  corresponding  part  will  be 
represented  bv  a  well-limited,  round  and  hard  nodule  (the 
capsule  remaining  tense). 

It  is  these  "tumors"'  which  wrongly  carrv  the  names  of 
"adenoma"  and  "adenomvoma,"  respectivelv. 

To  decide  why  sometimes  (in  the  so-called  diffuse  form 
of  hvpertrophy)  no  or  only  very  few  pseudo-adenomata 
are   formed,   one    must    make    investigations    especially 


directed  to  the  subject.  As  a  cause  of  the  so-called  diffuse 
form  may,  in  my  opinion,  be  taken  a  uniform,  very  ex- 
tensive but  relatively  weak  dilatation  of  the  gland,  such 
as  is  formed  in  consequence  of  a  very  early  narrowing  of 
the  main  excretory  duct,  just  at  its  outlet. 

If  several  pseudo-adenomata  be  formed  in  the  same 
part  of  the  prostate,  then  the  remaining  prostatic  will  be 
pushed  apart  by  them,  but  the  tissue  lying  between  them 
will  be  compressed.  In  such  cases  a  portion  of  the  gland 
ducts  still  at  the  end  absolutely  unchanged,  which  lie  next 
to  the  pseudo-adenomata,  will  be  in  layers,  sometimes 
much  so ;  the  glandular  parts  lying  between  two  growing 
pseudo-adenomata  will  be  compressed  and  narrowed ;  and 
it  may  lead  to  a  complete  obliteration :  in  the  latter  case 
a  gland  dilatation  in  the  peripheral  ramification  may  be 
the  consequence,  or  a  new  pseudo-adenoma  may  be 
formed.  In  this  way  a  pseudo-adenoma  may  cause  a 
further  enlargement  of  the  prostate  gland. 

But  the  pseudo-adenomata  may  themselves  be  displaced, 
they  may  partly  leave  their  point  of  origin  and  extend 
into  the  neighborhood  of  the  urethra,  i.  e.,  at  a  place 
where  normally  very  little  glandular  tissue  is  present. 
Why  and  how  the  pseudo-adenomata  come  to  lie  in  the 
neighborhood  of  the  urethra  will  be  made  plain  by  study- 
ing the  normal  prostate  gland,  which  was  especially  fully 
investigated  by  Aschoff  (2)  (on  complete  serial  section). 
Aschoff  demonstrated  that  the  main  excretory  ducts  of 
the  lateral  lobes  of  the  prostate  describe  a  long  curve  in  a 
direction  from  before  backwards  and  inwards,  i.  e.,  from 
the  symphysis  to  the  wall  of  the  rectum,  before  they  tc- 
minate  in  both  posterior  angles  of  the  urethra,  which  at 
this  level  is  triangular.  If  the  obstruction  to  the  outflow 
of  the  glandular  contents  be  situated  at  some  place  in  the 
main  excretory  duct,  then  the  gland  group  terminating  in 
the  main  duct  and  posteriorly  to  the  obstruction,  generally 
a  great  part  of  the  glandular  acini  of  one  of  the  lateral 
lobes,  will  suffer  a  dilatation  and  under  certain  circum- 
stances may  be  transformed  into  an  encapsulated  "pseudo- 
adenoma."  The  pseudo-adenoma  enlarges  them  more  and 
more,  in  that  it  grows  uniformly  in  all  directions,  pushing 
apart  the  surrounding  tissue.  But  finally  there  comes  a 
time  at  which  the  further  growth  of  the  pseudo-edenoma 
meets     with     great     resistance     from     without ;    this  is 


produced  by  the  capsule  of  the  prostate,  which  is  thick 
and  yields  only  slightly.  The  pseudo-adenoma  will  in  its 
further  growth  be  displaced  in  the  direction  of  the  lesser 
resistance,  i.  e.,  toward  the  lumen  of  the  urethra,  which 
is  pushed  in  front.  Little  by  little  it  fills  the  curve 
formed  by  the  main  excretory  duct,  and  finally  com- 
presses the  main  duct  in  its  whole  length,  whereby  the  out- 
flow of  the  secretions  becomes  more  and  more  hindered. 


I.  Fig.  2,  Fig.  3. 

Fig.  I.     Sche7natic  Horizontal  section   through    the  principal  excretory 

ducts  of  the  normal  prostate. 
Fig.  2.      Growing  Psendo-adeno7na.   (y^   Directio7i  of  Growth) 
Fig.  J.     A  large  Pseudo-adenoma  ( Displacement,   Arching  over   of  the 

wall  of  the  urethra. 

On  further  growth  the  pseudo-adenoma  causes  addi- 
tional changes.  If  in  the  opposite  lobe  of  the  prostate 
(at  the  same  level)  analogous  process  occurs,  then  the 
pseudo-adenomata  protruding  into  the  lumen  of  the 
urethra  must  both  flatten  themselves  against  each  other, 
and,  by  further  enlargement,  must  draw  the  lumen  length- 
wise in  a  sagittal  direction ;  but  if  the  opposite  lobe  of  the 
prostate  be  slightly  or  not  at  all  changed,  then  a  lateral 
deviation  of  the  urethra  at  the  level  of  the  pseudo- 
adenoma  will  be  the  consequence.  The  tumors  present  in 
the  vicinity  of  the  orificium  internum  urethra  were  also 
formed  in  consequence  of  the  dilatation  of  the  glandular 
acini  (which  in  the  majority  of  cases  are  to  be  found 
normal  at  the  place  under  consideration)  as  a  result  of 
the  restriction  or  obliteration  of  the  corresponding  ex- 
cretory ducts. 

The  relation  of  the  stroma  changes  to  the  secondary 
glandular  changes  is  more  difficult  to  demonstrate  a  this 
place  than  in  other  parts  of  the  prostate  gland,  except 
with  the  help  of  complete  serial  sections.  As  demon- 
strated by  Aschoff  (1.  c),  the  excretory  ducts  of  the 
gland  groups  imbedded  in  the  submucosa  above  the  col- 
liculus  seminalis  describe  a  long  way  beneath  the  mucou^ 
membrane  of  the  orifice  obliquely,   downward,   forward 


"3 


and  outward,  before  they  terminate  in  one  of  the  two 
posterior  angles  of  the  urethra.  But  ahhough  for  this 
reason  the  proof  of  the  causative  relation  of  the  stroma 
and  glandular  changes  does  not  always  succeed  here,  still 
both  will  be  found  side  by  side  in  one  and  the  same 
preparation.  The  stroma  changes  are  most  easily  to  be 
detected  when  they  appear  in  the  form  of  periglandular 
subepithelial  infiltrates ;  the  glandular  changes  have  also 
here  all  the  characteristics  as  described  before. 

It  still  remains  to  discuss  the  behavior  of  the  stroma 
muscle  tissue  of  the  enlarged  prostate  gland.  In  this  re- 
gard I  could  demonstrate  absolutely  only  two  conditions: 
the  absence  of  muscle  cells  in  the  vicinity  of  the  con.-tis. 
groups  scattered  in  the  stroma  and  the  transformation  of 
the  muscle  bundles  that  were  outwardly  displaced  into  a 
kind  of  concentric  capsule  enveloping  the  pseudo-ade- 
noma. Both  these  conditions  seem  to  indicate  that  the 
muscle  elements  play  an  entirely  passive  role  in  the  en- 
largement of  the  prostate.  The  function  of  the  prostate 
is  in  intimate  relation  to  the  sexual  function  ;  the  muscle 
tissue  of  the  stroma  seems  to  take  an  important  part  in 
this  function.  To  it  falls  the  work  of  propelling  the 
contents  of  the  gland  acini  outward.  If  the  outflow  of 
the  secretion  meets  with  any  obstruction,  the  muscle  tissue 
of  the  corresponding  part  of  the  prostate  must  then  suffer 
a  working  hypertrophy,  provided  that  the  sexual  func- 
tions and  with  them  the  specific  function  of  the  prostate 
be  retained  within  physiological  limits.  It  is  to  be  re- 
gretted that  no  method  is  at  our  disposal  by  which  we 
might  detect  if  and  in  what  way  such  a  working  hyper- 
trophy is  really  formed  here ;  however,  I  have  the  impres- 
sion that  in  prostate  glands  that  are  much  enlarged  the 
peripheral  fibromuscular  capsule,  which  envelops  the 
whole  organ,  is  much  thicker  than  in  the  normal  ones. 

The  view  is  quite  common  that  the  individuals  afflicted 
with  "hypertrophy"  of  the  prostate  are  too  old  to  expect 
in  them  any  function  of  the  already  atrophic  sexual  or- 
g"ans.  In  particular  the  adherents  of  castration  as  the 
treatment  for  prostate  hypertrophy  seek  justification  for 
the  mutilating  operation  in  this  view.  If  this  were  the 
ease,  it  were  then,  "a.  priori,"  to  be  presumed  that  an  active 
hypertrophy. of  the  muscle  tissue  of  the  prostate  is  not  at 
all  conceivable  in  an  enlargement  of  the  prostate.     Such  a 

114 


conclusion  would  be  just  as  wrong  as  the  premises  which 
serve  as  its  support.  In  this  regard  it  may  suffice  to  refer 
to  the  results  cited  by  Hoffmann  (Lehrb.  der  gerichtl. 
Medizin,  6  aufl.,  1893,  p.  59)  of  the  investigations  made 
by  Duplay  (Arch.  gen.  de  Med.,  Decembre,  1852)  and 
Dien  (Journ.  de  I'anatomie  et  de  la  physiologic.  1867,  p. 
449).  Duplay  found  among  51  corpses  of  old  people 
spermatozoa  in  37,  occurring  in  23  of  these  in  consider- 
able amounts.  Dien,  who  examined  105  corpses  of  old 
men,  demonstrated  the  presence  of  spermatozoa : 

Between  the    64th  and  the  70th  Year  of  life  14  cases  in  64.3  percent 

70         "     "     80  "       "     "  4Q  "       ■'  44. S         " 

"         "      80         "     "    90  "       "     "  38  "       "  26.3 

"      9°         "     "    97  "       "     "  4  "       "             not  once 

From  this  investig^.tion  it  can  be  seen  that  atrophy  of 
the  sexual  organs  and  the  cessation  of  the  function  in  old 
men  neither  occurs  so  frequently  nor  appears  so  early  as 
is  generally  assumed.  The  possibility  of  the  active  hyper- 
trophy of  the  muscle  tissue  of  the  prostate  must  not, 
therefore,  "a  priori,"  be  cast  aside.  There  even  exists  in 
the  literature  a  hypothesis  verified,  however,  by  no  one, 
that  the  "hypertrophy"  of  the  prostate  gland  depends 
upon  an  active  hypertrophy  of  the  muscle  tissue  of  the 
prostate. 

Stilling-  (120),  during  his  investigations  of  the  causes 
of  the  formation  and  enlargement  of  the  amyloid  bodies, 
conceived  the  idea  that  they  stand  in  an  intimate  relation 
to  the  stagnation  of  the  elements  which  serve  to  build  up 
the  amyloid  bodies  in  the  lumen  of  the  prostate  gland, 
whether  it  be  in  consequence  of  a  hyaline  degeneration,  or 
whether  it  he  in  consequence  of  the  narrozving  or  ohlitera^ 
tion  of  the  excretory  ducts  (1.  c.  p.  19).  These  changes 
which  produce  a  narrowing  or  an  obliteration  of  the  ex- 
cretory ducts  were  regarded  by  Stilling  as  a  process  re- 
lated to  the  "Myxangoitis  hyalinosa"  of  Recklinghausen 
(Virch.,  Arch..  Bd.  84.  p.  479)  ;  imder  certain  conditions, 
according  to  Stilling,  in  the  obstruction  produced  by  it 
to  the  outflow  of  the  prostate  secretion  is  to  be  sought  the 
cause  of  an  active  hypertrophy  of  the  muscle  tissue  of  the 
prostate,  followed  by  an  enlargement  of  the  entire  prostate 
gland  (1.  c.  p.  20-21).  The  latter  hypothesis  of  Stilling 
is  on  no  point  verified  by  my  investigations.  On  the  con- 
trary, from  the  description  and  the  accompanying  illus- 
trations, it  is  unquestionably  to  be  seen  that  the  changes 


observed  by  Stilling  (Myxangoitis  hyalinosa)  are  entirely 
identical  with  the  periglandular  cicatricial  groups  de- 
scribed by  me.  Neither  were  the  stroma  changes  de- 
scribed by  me  entirely  overlooked  by  some  other  investi- 
gators, but  still  no  importance  was  attributed  to  them. 
Aside  from  the  views  already  mentioned  (p.  iii)  of 
Rindfleisch  (311),  "round-cell  accumulations"  find  only 
a  superficial  mention  in  the  works  of  Casper  (16,  p.  157), 
Jores  (63,  p.  241)  and  Motz  (89b).  This  is  all  I  could 
find  about  it  in  the  literature. 

During  my  studies  I  also  examined  a  series  of  twenty- 
two  apparently  normal  prostate  glands,  of  normal  weight, 
normal  form  and  normal  dimensions,  which  were  taken 
either  from  old  individuals  attacked  by  an  extensive 
atheromatosis  or  from  young  men :  in  several  of  these 
cases  I  could  not  demonstrate  any  pathological  changes. 

There  were  twelve  in  which  the  prostate  gland  proved 
to  be  entirely  normal,  and  two  in  which,  aside  from 
a  subepithelial,  round-cell  infiltrate  distributed  patch- 
like in  the  urethra  no  other  changes  were  found  in  the 
vicinity  of  the  prostate  gland ;  that  is,  in  14  cases  all  told. 

Aside  from  these  I  met  with  a  few  examples  which  did 
not  exceed  the  upper  normal  limit,  but  the  structure  of 
which  nevertheless  showed  pathological  changes. 

Case  No.  22     45  Years   old  Weight  of  the  Prostate  17.5  g 

1'       "      ,,     c       '<         '<  n         "     "         "  jgo  n 

"  "  "  15.5 

"  "  "  16.8 

"  "  "  19.1 

"  "  17.5 


2  " 

3  " 

4  " 

'   31  57   " 
'   36  70   " 
'   39  60   "    ' 

5 
6 

'   4°  70   " 
'   47  56   " 

7 

8    " 

'   29  75   " 

15-4 
18.0 


One  served  as  a  type  of  the  first  stage  of  the 
"hypertrophy"  of  the  prostate.  In  the  remaining  cases 
an  entirely  analogous  condition  might  be  demonstrated 
partly,  as,  for  instance,  one  case,  in  which  one  likewise  en- 
countered a  wedge-shaped  part  of  the  gland :  in  the  vicin- 
ity of  this  part  the  empty  spaces  were  moderately  dilated 
and,  in  the  apex,  pointed  toward  the  centre  of  the  pros- 
tate, a  round-cell  infiltrate  was  visible  surrounding  the 
excretory  duct.  In  three  other  cases  the  changes  were 
still  more  insignificant,  in  that  they  consisted  en- 
tirely of  a  few  moderately  small  round-cell  infiltrates, 
which  were  situated  mainly  in  the  neighborhood  of 
the  ramifications  of  the  peripheral  gland.  Therefore 
it  cannot  be  decided  whether    in    these    three    cases    a 

116 


high-grade  glandular  dilatation  could  have  been  formed 
later  on,  in  consequence  of  a  damming  back  of  the  secre- 
tion. The  possibility  of  such  an  outcome  could  not  be 
passed  over  unnoticed,  at  least  in  young  individuals, 
as  there  already  existed  in  the  prostate  gland  a  related 
pathogenetic  irritation,  and  a  further  spreading  is  quite 
conceivable. 

Of  the  three  remaining  cases,  in  one  there  were 
to  be  found  changes  which,  although  insignificant, 
are  yet  especially  interesting.  In  the  kimen  of  the 
dilated  glandular  acini  (of  which  there  were  only  a  few) 
one  encountered  numerous  leucocytes ;  the  contents  of 
one  of  the  gland  acini  had  even  the  characteristics  of  a 
genuine  suppurative  exudate.  Finally,  in  the  two  cases 
high-grade  changes  were  encountered ;  in  both  a  few 
small  pseudo-adenomata  were  formed.  Although  they 
were  still  in  so  early  a  stage  of  development  that 
they  could  not  influence  the  dimensions  of  the  pros- 
tate gland,  yet  these  two  cases,  as  well  as  the  other  six, 
must  be  regarded  as  pathological.  It  has  been  already 
demonstrated,  however,  by  Thompson  that  sometimes 
limited,  easily  enucleated  nodules  were  found  in  prostate 
glands  not  at  all  enlarged ;  similar  cases  were  also  ob- 
served by  Iversen  ( [64]  schematic  review  of  cases,  p.  18, 
a.  s.  f.) 

The  cases  last  mentioned  seem  to  prove  that  the  spe- 
cific changes  for  the  "hypertrophy"  of  the  prostate  may 
persist  for  a  long  time  in  their  low  grades  before  they 
become  visible  to  the  naked  eye.  This  also  conforms  to 
the  view  of  some  investigators  who  place  the  beginning  of 
the  "hypertrophy"  of  the  prostate  gland  at  a  much  earlier 
time  than  is  generally  assumed.  Among  the  individuals 
in  whom  I  was  able  to  demonstrate  the  histological 
changes  in  a  prostate  gland  that  was  not  enlarged  were  a 
few  who  had  hardly  passed  the  forty-fifth  year  of  life; 
one  of  them  was  even  not  quite  forty  years  old. 

By  further  exact  investigation  of  prostate  glands  that 
are  not  enlarged  the  proof  will  without  doubt  be  obtained 
that  the  cases  in  which  the  pathological  changes  already 
exist,  although  they  are  not  discerned  with  the  naked  eye, 
are  much  more  frequent  than  would  appear  from  the 
statistical  data  of  Thomson  and  Iverson.  One  will  in  all 
probability  find  that  the  beginning  of  the  changes  is  to 

117 


be  placed  at  a  much  earlier  time  than  would  appear  from 
my  investigation. 

Among  the  prostate  glands  examined  by  me  there  were 
nine  (from  individuals  well  developed  sexually)  which 
weighed  less  than  normal :  among  these  three  weighed 
I4-I4.6g.,  the  remaining  hardly  i2-i3g.  In  four  of  these 
small  prostate  glands  I  encountered  changes  which  were 
entirely  in  conformity  with  the  prevailing  views  of  the 
simple  atrophy  of  the  prostate. 

No.  20  Age  65  Years.  Weight  of  the  Prostate  12.0  g 

"     21  "  75      "  "         "     ■•         "           12.5  " 

26  "  42      "  "         "     "         "           13.2  " 

"     33  "  62      "  "         "     "         "           12.0  " 

The  changes  here  observed  consisted  exclusively  in  a 
diminution  of  the  glandular  ramifications  ( decrease  of  the 
gland  tubuli)  and  in  the  presence  of  amyloid  bodies.  The 
gland  tubuli  still  preserved  were  nowhere  plainly  dilated ; 
in  the  stroma  there  were  no  changes  of  any  importance. 
The  histological  picture  corresponds  in  the  main  to  that 
of  an  atrophy  of  the  prostate  gland,  which  is  experi- 
mentally produced  in  animals  by  castration ;  and  this 
seems  to  indicate  that  under  ordinary  circumstances 
trophy  attacks  first  the  gland  tubuli. 

But  the  matter  was  dififerent  in  the  remaining  five 
cases.     I  was  much  surprised  when   it  appeared  that  in 


No.  23 

Age 

57  Years, 

Weight  of  the  Prostate  14.0  g 

"     30 

40      •' 

'■         "     "         •■           12.4  " 

"    32 

" 

70      " 

"         "     "         "           12.5  " 

"     35 
"     38 

'•' 

72      " 
62      " 

"         "     "         "           14.6  " 
"         "     "         "           14.2  " 

these  five  cases  the  changes  in  the  individual  parts  of  the 
structure  were  exactly  like  those  observed  in  the  "hyper- 
trophy" of  the  prostate.  Here,  as  there,  at  least  in  some 
parts  of  the  gland,  a  pathological  contents  was  present 
composed  of  changed,  desquamated  epithelium,  sometimes 
with  an  addition  of  leucocytes.  Likewise  we  also  en- 
counter, at  least  here  and  there,  dilated  glandular  acini  or 
small  pseudo-adenomata,  although  in  a  mild  degree. 
Above  all,  we  encountered  similar  stroma  changes,  which 
appear  sometimes  in  the  form  of  small-cell  infiltrates, 
sometimes  as  spindle-cell  con.-tis.  groups ;  but  usually  in 
the  form  of  numerous  patchy  cicatrices,  which  we  have 
learned  to  know  in  the  enlarged  prostate  ghnd.  In  the 
cicatricial  groups  were  sometimes  found  remains  of  gland 
tumuli  with  a  few  epithelial  cells  or  narrowed  lumina  de- 
prived of  their  epithelium,  or  apparently  loosely  deposited 

118 


amyloid  bodies;  but  these  cicatrices  had,  for  the  greater 
part,  a  uniform  structure. 

At  first  I  was  not  able  to  find  a  sufficient  explanation 
for  such  pictures.  The  supposition  ready  to  hand^  that 
this  is  the  remains  of  the  processes  of  the  specific  changes 
for  the  enlargement  of  the  prostate  after  a  spontaneous 
reversion,  is,  however,  hardly  tenable ;  because  nobody 
ever  observed,  to  my  knowledge,  that  a  "hypertrophy"  of 
the  prostate  spontaneously  reversed ;  yes,  even  more,  was 
able  to  change  to  an  opposite  condition,  namelv,  atrophy. 

Only  after  an  exact  consideration  of  all  the  histological 
facts  was  I  convinced  that  the  presence  of  these  changes 
in  the  individual  structures  of  the  stroma  stands  in  no 
opposition  to  the  diminution  of  the  WHOLE  prostate 
gland ;  yes,  further,  they  may,  on  the  contrary,  be  useful 
for  the  elucidation  of  hypertrophv  of  the  prostate,  al- 
though these  changes  are  apparently  inseparably  con- 
nected with  "hypertrophy."  In  other  words,  it  is  proved 
that  the  localisation  of  the  changes  and  their  distribution 
between  the  two  main  component  parts  of  the  prostate, 
the  glandular  tissue  and  the  stroma,  is  different  in  cases 
of  atrophy  of  the  prostate  from  the  "hypertrophy,"  and 
that  the  main  difference  lies  in  the  location  of  the  lesions. 

One  encounters  here  mainly  the  cicatricial  tissue,  to 
the  shrinkage  of  which  the  diminution  of  the  whole 
of  the  prostate  gland  is  to  be  referred :  these  cicatri- 
cial groups  are  very  numerous.  The  shrinkage  is  a 
consequence  of  the  changes  in  the  stroma,  which  have 
left  unaffected  the  vicinity  of  the  main  excretory  ducts 
and  have  mainly  extended  to  the  neig-h'^orhood  of  the 
terminal  ramifications  of  the  gland  tubuli.  The  stroma 
changes  have  here,  as  everywhere  else  where  they  are 
formed,  the  narrowing,  the  obliteration  and  the  atrophy 
of  the  glandular  acini  as  a  consequence.  But  because  all 
these  changes  mainly,  or  perhaps  exclusively,  include  the 
blind  ends  of  the  glandular  systems,  they  were  not  able 
to  hinder  the  outflow  of  the  contents  from  the  still  pre- 
served central  parts  of  the  gland  tubuli. 

The  dilated  gland  acini  are  therefore  found  onlv  in  a 
few  places,  where  a  scattered  con.-tis.  group  had  sur- 
rounded accidentally  one  of  the  larger  excretorv  ducts. 
A  gland  dilatation  which  included  onlv  a  verv  small  part 
of  the  prostate  was  not  able  to  produce  a  visible  enlarge- 

119 


merit  of  the  whole  organ.  To  this  it  is  due  that  an  in- 
significant increase  m  the  volume  of  individual  glandular 
systems  could  be  compensated  by  the  atrophic  changes  in 
other  parts  of  the  prostate,  and  finally  that  these  could 
more  tnan  counterbalance  it. 

By  this  it  is  made  more  clear  why  in  some  prostate 
glands  quite  extensive  "hypertrophic"  changes,  i.  e.,  the 
relatively  great  dilatation  of  several  glandular  acini  and 
a  relatively  abundant  formation  of  con.-tis.  masses,  could 
be  present  in  the  stroma  without  the  weight  and  size  of 
the  whole  prostate  gland  exceeding  the  normal  limits. 

The  so-called  hypertrophy  of  the  prostate  gland,  as 
well  as  certain  forms  of  prostatic  atrophy  which  are  histo- 
genetically  related  to  it,  have  a  common  origin.  Both 
these  processes  differentiate  themselves  from  each  other 
not  through  the  quality  of  the  changes  of  their  structures, 
but  onlv  through  the  different  extension,  intensity,  and, 
above  all,  through  the  different  distribution  and  localiza- 
tion of  otherwise  analogous  changes. 

The  common  starting-point  of  the  hypertrophy  of  the 
prostate  gland  and  certain  forms  of  atrophy  must  be 
sought  in  the  productive  connective-tissue  processes  which 
have  their  seat  in  the  stroma  of  the  organ  ;  and,  according 
to  the  stages  of  their  development,  they  may  show  the 
different  forms  of  organization  of  the  connective-tissue 
which  occur  constantly  multiple  and  mainly  close  by  the 
glandular  epithelium. 

If  the  productive  stroma  changes  localize  themselves  in 
the  central  parts  of  the  prostate  in  the  vicinity  of  the  main 
excretory  duct,  then  it  may  be  possible  that  they  produce 
a  narrowing  or  obliteration  of  the  lumen  of  this  duct, 
which  may  cause  an  accumulation  of  the  secretion  and  an 
enlargement  of  the  peripheral  lobules.  The  enlargement 
of  the  lobules  is  produced  more  quickly  and  is  of  a  higher 
degree  according  as  the  excretory  ducts  are  more  nu- 
merous and  are  nearer  to  the  obstacle ;  furthermore,  the 
greater  the  extent  and  intensity  of  the  endoglandular 
pathological  process,  which  is  adjacent  and  is  always  pres- 
ent at  the  same  time,  the  greater  is  the  enlargement. 

These  processes  consist  of  a  very  active  proliferation, 
besides  a  desquamation  and  degeneration  of  the  epithelium 
which  characterize  it  as  a  catarrhal  process ;  sometimes 
there  is  in  addition  a  suppurative  process  which  causes  an 


addition  of  leucocytes  to  the  excretion  of  the  gland.  The 
enlargement  of  the  prostate  gland  is  nearly  always  to  be 
referred  to  the  enlargement  of  the  acini;  the  relatively 
large  masses  of  new-formed  connective-tissue  play  a  sub- 
ordinate part  in  the  pathological  growth  of  the  prostate 
gland.  The  active  role  of  the  prostatic  muscle  in  forms  of 
hypertrophy  of  the  prostate  gland,  without  formation  of 
genume  myomata— and  that  is  the  condition  in  the  ma- 
jority of  cases — is  not  proved  and  is  very  doubtful. 

If  the  connective-tissue  changes  in  the  stroma  occupy 
mamly  the  peripheral  part,  and  if  they  localize  themselves 
m  the  neighborhood  of  the  terminal  branches  of  the 
tubules  of  the  acini ;  then,  by  the  adhesion  and  atrophy  of 
the  compressed  tubules  and  by  a  shrinkage  of  the  connec- 
tive-tissue in  the  stroma— a  prostatic  atrophy— there  will 
be  produced  a  diminution  of  the  whole  organ.  This  dimi- 
nution will  be  the  quicker  and  more  intense  if  no  endo- 
glandular  pathological  process,  which  increases  the  con- 
tents of  the  acini,  be  present. 

Besides  there  are  also  simple  atrophies  of  the  prostate 
gland,  which  may  be  referred  to  a  process  of  involution 
within  the  glandular  tissue. 

If  the  pathological  changes  take  up  about  evenlv  both 
main  divisions  of  the  prostatic  tissue,  and  if  they  are 
situated  partly  in  the  periphery  antd  partly  in  the  central 
portion  of  the  prostate  gland,  then  it  may  be  possible  that 
the  different  localized  processes  may  compensate  each 
other  and  may  retain  the  normal  weight  of  the  prostate  ; 
or  if  one  of  these  two  processes  gains  the  upper  hand,  the 
prostate  gland  as  a  whole  will  become  smaller  or  larger, 
as  the  case  may  be. 

^^  The  intimate  histogenetic  relationship  of  the  so-called 
hypertrophy"  of  the  prostate  gland  and  certains  forms  of 
prostatic  atrophy  tends  to  show  that  between  these  two 
processes  there  may  exist  an  etiological  intimate  relation- 
ship. 


CHAPTER    IX. 

ETIOLOGY     OF     THE      SO=CALLED     "HYPER= 

TROPHY  OF  THE  PROSTATE"  AND 

CERTAIN    FORnS    OF  ATROPHY 

OF     THE     PROSTATE 

Since  it  was  demonstrated  in  the  last  chapter  that  the 
hypertrophy  of  the  prostate  in  the  majority  of  cases  has 
nothing  to  do  with  a  new  formation,  in  a  hmited  sense  of 
the  words,  it  does  not  seem  necessary  to  recapitulate  the 
views  in  regard  to  it  as  held  by  the  different  investigators 
(Cohnheim  [29a],  Socin  [119], -Birch-Hirschfeld  [297], 
Iversen  [64],  Maas  [84],  Kleb  [305],  Albert  [i],  Thomp- 
son [133],  Jores  [68],  Griffith,  and  many  others). 

The  statement  that  the  hypertrophy  of  the  prostate  is 
to  be  regarded  as  a  senile  involution  of  the  prostate  gland 
in  a  physiological  sense  is  mainly  advocated  by  the  French 
authors  (Cornil  and  Rauvier  [289],  Regnault  [114], 
Launois  [72],  Guyon  [406],  Miguel  [87],  the  last  three 
with  regard  to  the  arterio-athernoma,  and  further  Stock- 
ton-Hough [125]  and  many  others).  One  would  think 
that  such  views  were  long  ago  discarded  in  consideration 
of  the  statistics  of  Dittel  (23)  and  Thompson  (132)  and 
the  daily  experiences.  As  the  "hypertrophy"  of  the  pros- 
tate is  not  constantly  to  be  observed  in  old  age,  and,  on 
the  other  hand,  is  sometimes  demonstrated  in  relatively 
young  individuals  (40-45  years),  it  can  by  no  means  pass 
for  a  physiological,  senile  phenomenon.  Nevertheless, 
this  view,  although  in  a  quite  modified  form,  begins  to 
take  hold  anew.  For  instance,  it  was  demonstrated  by 
the  clinical  observations  and  anatomical  investigations  of 
Launois  {/t,)  and  Englisch   (374)  that  the  development 


and  function  of  the  prostate  stand  in  a  certain  relation  to 
the  testicle. 

The  experiments  on  animals  executed  by  Griffiths  (55, 
386),  Ramm  (comp.  447-478},  White  (comp.  521-6), 
Leyuen  (81),  Pavone  (after  81),  Latis  (19),  Lesine 
(71a),  Przewalski  (107),  Casper  (16a),  Sackuhr  (after 
i6a)  and  Floderus  (35a)  furnished  the  proof  that  cas- 
tration nearly  constantly,  and  resection  of  the  vas  deferens 
in  a  fraction  of  the  cases,  have  an  atrophy  of  the  normal 
prostate  as  a  consecjuence.  Finally,  it  was  proved  by 
clinical  observations  that  in  a  part  of  the  cases  the  hyper- 
trophy of  the  prostate  could  be  decreased  in  man  by  cas- 
tration. It  is  proved  by  all  these  facts  that  the  period  of 
development  of  the  prostate  is  parallel,  up  to  a  certain 
time,  with  that  of  the  testicle,  and  is  dependent  on  it ;  and 
that  the  function  of  the  prostate  may  be  brought  to  a 
stop  by  castration,  but  only  if  the  prostate  gland  was  pre- 
viously unchanged  (experiments,  on  animals).  To  this 
conclusion  all  cautious  investigators  come  without  de- 
ducing any  further  consequence.  But  not  all  are  so  cau- 
tious. Some  authors  believe,  namely,  that  they  are  justi- 
fied by  the  facts  cited  in  making  the  statement  that  the 
testicles  alone  are  capable  of  producing  the  "hyper- 
trophy" of  the  prostate  gland  (Moullin  Mansell  [93,  436], 
Latis  [79],  Launois  [73],  and  with  the  addition  of  the 
influences  of  sexual  excess,  Lydston  [80]).. 

At  present  MacEwan  (89c,  p.  769)  refers  the  prostate 
hypertrophy  to  the  atrophy  of  the  testicles  apparently  oc- 
curring in  old  age  and  to  the  insufficiency  resulting  from 
it  of  an  "internal  secretion"  of  the  testicle,  which  is  sup- 
posed to  regulate  the  period  of  development  and  function 
of  the  prostate.  In  general,  the  etiology  of  the  "hyper- 
trophy" of  the  prostate  is  also  referred  by  this  investigator 
to  senile  influences,  and  between  these  two  ideas  a  con- 
necting link  is  introduced,  namely,  the  senile  atrophy  of 
the  testicle. 

Through  another  still  unfinished  work  I  might  dem- 
onstrate that  the  development  of  the  prostate  really  runs 
parallel  with  that  of  the  testicle,  and  that  the  atrophy  of 
the  testicle  really  causes  changes  in  the  prostate  which 
later  by  no  means  take  the  form  of  a  paradoxical  phe- 
nomenon, i.  e.,  the  enlargement  of  the  prostate,  but  take 
the  -form  cif  the  simj^le  atrophy  already  described. 


123 


The  enlargement  of  the  prostate  in  old  people  sometimes, 
but  by  no  means  constantly  encountered,  is,  as  I  shall  have 
the  opportunity  to  demonstrate  in  another  way,  an  entirely 
accidental  morbid  complication,  which  covers  only  the 
normal  period  of  development  and  the  simple  atrophy,  re- 
spectively, of  the  sexual  organs.  But  before  I  give  the 
results  of  my  investigations  on  this  point,  the  facts  already 
known  and  demonstrated  may  be  of  use  for  the  elucida- 
tion of  the  question  under  consideration. 

One  can,  of  course,  overlook  the  statement  that  the 
human  prostate  is  in  a  state  of  continuous  growth  up  to 
the  highest  age  (Regnault  [114],  Launois  [73]),  as  this 
statement  is  in  plain  opposition  to  the  fact  that  the  pros- 
tate gland  shows  no  enlargement  in  the  majority  of  old 
people. 

The  investigation  based  on  the  statistics  taken  from 
living  persons  by  Englisch  (374)  cannot,  for  obvious  rea- 
sons, be  regarded  as  exact. 

By  the  observation  that  above  a  certain  age  there  is  a 
prostate  enlargement  in  every  second  or  third  individual, 
no  proof  is  furnished  that  the  greater  "development"  of 
the  prostate  gland,  in  proportion  to  the  size  of  the  testicle, 
is  physiological. 

The  adherents  of  the  theory  according  to  which  the 
"hypertrophy"  of  the  prostate  is  caused  by  a  weakening 
and  cessation,  respectively,  of  the  function  of  the  testicle, 
contradict  themselves  with  their  own  views.  First,  they 
give  as  proof  of  an  intimate  relation  between  the  period 
of  development  of  'the  prostate  and  the  testicles,  the  fact 
that  castration  causes  an  atrophy  of  the  prostate  by  elimi- 
nating the  sexual  function,  and  then,  again,  they  main- 
tain that  the  hypertrophy  of  the  prostate  is  a  consequence 
of  the  elimination  of  the  sexual  function.  How  can  the 
adherents  of  this  theory  explain  the  observation  of  Moses 
(444),  who  demonstrated  in  a  sixty-eight-year-old  man  a 
"hypertrophv''  of  the  prostate  occurring  several  years 
after  a  double  castration  ?  Where,  in  this  case,  is  the 
cause  of  the  "hypertrophy"  to  be  sought,  when  the  cessa- 
tion of  the  sexual  function  should  have  caused  an  atrophy 
already  several  years  before?  This  case  does  not  seem  at 
all  mysterious  if  we  look  back  to  our  previously  repre- 
sented histological  investigation.  The  characteristic 
changes  in  the  tissues  of  the  prostate  have  developed  in- 

124 


dependently  of  the  presence  or  absence  of  the  testicles. 

In  the  discussion  of  the  importance  of  the  cessation  of 
the  functions  and  atrophy  of  the  testicles  for  the  origin 
of  the  hypertrophy  of  the  prostate  Launois  (73)  cites  the 
works  of  Monod  and  Serillon  (88,  89)  and  Arthaud  (3), 
who  dealt  with  the  senile  changes  of  the  testicles.    But  he 
does  not  mention  the  work  of  Desnos   (25),  who  dem- 
onstrated that  among  one  hundred  and  twenty  old  people 
living  spermatozoa  were  found  in  one-half  of  the  cases. 
If  the  spermatozoa  were  missing  in  one  of  the  seminal 
vesicles,  then  this  was  not  dependent  upon  an  atrophy  of 
the  testicle,  but  upon  an  obliteration  of  the  seminal  ducts. 
The  atrophy  of  the  testicle  itself  is  not  produced,  how- 
ever, by  the  influence  of  age,  but  probably  by  other  very 
varied   causes.      These   investigations   coincide   with   the 
older  investigations  already  mentioned   (cit.  after  Hoff- 
mann.     See  p.  121  in  MS.).     By  them  it  is  at  any  rate 
proved  that  the  atrophy  of  the  testicles  and  the  cessa- 
tion of  the  sexual  function  is  much  rarer  than  the  "hyper- 
trophy" of  the  prostate  in  old  people,  and,  therefore,  can- 
not be  regarded  as  a  cause  for  the  enlargement  of  the 
prostate.     The  fact  was  also  put  forth  that  the  prostate 
gland  in  animals  normally  enlarges  continually  up  to  the 
highest_  age    (Regnault    [114)].     Disregarding  the  fact 
that  it  is  not  allowable  to  transfer  to  man  the  results  of 
investigations  made  on   animals,   it  must  be  considered 
that  the  obsevations  were  entirely  based  upon  investiga- 
tions made  on  dogs.     This  species  of  animals  seems  to 
occupy  an  exceptional  place  with  regard  to  the  prostate, 
as    castration,    which    constantly    produces    pronounced 
atrophy  of  the  prostate  in  other  animals  (rabbits),  gave 
very  varied  and  sometimes  even  directly  contradicting  re- 
sults in  dogs.     I  have  already  mentioned  (p.  58  in  MS.) 
the  fact  demonstrated  by  Casper  (i6a),  that  the  atrophy 
of  the  prostate  after  castration  is  less  pronounced  in  dogs 
than  in  rabbits.     Leguen   (81)    did  not  succeed  in  pro- 
ducing an   atrophy   of  the  prostate  gland  by  a  double 
vasectomy  in  five  out  of  six  dogs  operated  upon.    A  very 
old  dog,  killed  five  months  after  the  operation,  had  after 
as  well  as  before  the  operation  a  very  large  prostate  gland. 
This  failure  seems  not  to  be  dependent  on  the  kind  of 
operation,  as  in  the  sixth  dog  a  pronounced  atrophy  of 
the  prostate  occurred  several  days  after  the  operation. 

"5 


It  seems  from  these  experiments  that  dogs  really  occupy  a 
special  place  among  the  mammals.  Agreeing  with  this,  it 
is  stated  in  several  veterinary  manuals  (Bruckmiiller 
[315],  Forster  [317],  Koch  [318],  Konhaiiser  [319], 
Moller  [320],  Roll  [321],  Stockfleth  [322])  that  inflam- 
mation of  the  prostate  and  hypertrophy  of  the  prostate, 
similar  in  several  respects  to  the  human,  are  among  all 
the  domestic  animals  observed  only  in  dogs.  In  the  other 
domestic  animals  the  "hypertrophy"  of  the  prostate  has 
not  been  generally  observed,  and  the  prostate  enlarge- 
ments— by  the  way,  very  rare — were  to  be  referred  to 
genuine,  mostly  malignant,  tumors. 

"Hypertrophy"  of  the  prostate  gland  seems,  then,  to  be 
a  specific  disease  found  solely  in  man  and  in  dogs ;  where- 
fore the  experiments  made  on  dogs  must  give  just  as  am- 
biguous results  as  the  experiences  gained  from  man.  But, 
at  any  rate,  these  results  were  not  adapted  to  prove  that 
the  prostate  of  animals  continues  to  enlarge  up  to  the 
time  of  death ;  because  the  large  prostate  glands  found  in 
old  dogs  were  only  pathologically  '"hypertrophied,"  and 
the  physiological  enlargement  of  the  prostate  in  advanced 
age  of  other  species  of  animal  is  still  not  proved  by  any 
one.  Therefore,  the  assertion  that  the  "hypertrophy"  of 
the  prostate  is  produced  by  the  cessation  of  the  sexual 
function  due  to  an  atrophy  of  the  testicles  must  be  aban- 
doned. 

Finally,  the  opinion  advocated  in  the  literature  here  and 
there  may  be  cited  that  inflammatory  processes  play  a 
causative  role  in  the  formation  of  the  "hypertrophy"  of 
the  prostate.  Such  influences  were  formerly  very  fre- 
quently cited  among  the  causes  of  the  "hypertrophy  of 
the  prostate" ;  but  as  later  on  the  chronic  inflammation  of 
the  prostate  (prostatitis  chronica)  was  separated  from 
the  "hypertrophy"  of  the  prostate,  from  a  clinical  stand- 
point it  was  almost  generally  accepted  that  the  latter 
never  stands  in  a  causative  relation  with  the  passed  in- 
flammatory processes.  This  exclusive  standpoint  is  very 
energetically  taken  and  defended  by  all  clinicians,  al- 
though it  really  is  no  longer  attacked  by  any  one.  Once 
in  a  while  we  encounter  in  some  manual  or  in  a  casuistic 
work  a  cursorv  remark  that,  besides  other  influences,  pcv- 
haps  inflammatory  factors  also  may  sometimes  play  a  role 
in  the  etiology  of  "hypertrophy  of  the  prostate."     The 

126 


objection  advanced  from  a  clinical  standpoint  against  the 
causative  relation  of  the  "hypertrophy  of  the  prostate"  to 
inflammatory  processes  can  be  summed  up  in  the  follow- 
ing sentences  :  ( i )  The  anamnestic  data  which  would 
point  to  passed  inflammatory  processes  are  missing  in 
the  patients  suffering  from  "hypertrophy"  of  the  prostate. 
No  great  importance  should,  in  my  opinion,  be  given  to 
this  circumstance,  as  the  anamnestic  data  may  be  incom- 
plete or  inexact ;  because,  as  I  shall  demonstrate  later,  the 
inflammatory  processes  of  the  sexual  organs  may  run  a 
latent  course.  (2)  The  clinical  course  of  the  chronic 
prostatitis  is  entirely  different  from  that  of  the  hyper- 
trophy of  the  prostate  gland.  How  little  weight  can  be 
laid  upon  such  an  objection  is  shown  by  the  countless 
diseases  of  other  organs,  generally  known,  which  may 
have  a  common  etiology  and  an  entirely  different  clinical 
picture.  As  an  example  we  may  cite  a  valvular  lesion, 
caused  by  articular  rheumatism,  and  first  noticed  several 
years  later.  I  believe  that  a  causative  relation  between 
these  two  processes  will  hardly  be  doubted  by  any  one. 
Or  has,  for  example,  syphilis  of  the  central  nervous  sys- 
tem, any  similarity  to  the  common  manifestations  of  this 
infection?  (3)  The  third  objection  rests  upon  a  conclu- 
sion from  analogy :  "Other  experiences  also  show  that 
repeated  acute  or  chronic  inflammatory  processes  of 
glandular  tissue,  after  they  have  run  their  course,  will 
lead  to  an  atrophy  sooner  than  to  a  hyperplastic  tumor 
formation"  (Socin  [119,  p.  51])-  This  view,  which  is  in 
the  main  correct,  can  find  no  special  application  with  re- 
gard to  the  prostate  gland  :  first,  because,  as  has  been  dem- 
onstrated in  this  work,  the  "hypertrophy"  of  the  pros- 
tate must  not  be  regarded  as  a  "hyperplastic  tumor  for- 
mation," and,  secondly,  because  the  prostate  is  undoubt- 
edly a  gland,  but  a  gland  the  structure  of  which  is  not 
comparable  to  any  others  found  in  the  organism. 

The  contraction  of  the  cicatricial  tissue  may  here,  as 
anywhere  else,  have  very  different  consequences,  accord- 
ing to  the  extent  and  localization  of  the  cicatrices.  Here 
may  be  mentioned  the  cicatricial  strictures  of  the  pylorus 
after  a  round  ulcer,  which  are  followed  by  a  dilatation 
and  compensating  hypertrophy;  while  a  cicatrix  at  any 
other  place  of  the  stomach  is  not  followed  by  similar  con- 
ditions. 


127 


To  my  knowledge,  only  Casper  tried  to  refute,  on  the 
basis  of  anatomical  investigations,  the  relation  of  the 
"hypertrophy"  of  the  prostate  (that,  namely,  which  he 
described  as  "Hypertrophia  prostat?e  fibromyomatosa  vel 
fibroma  diffusum  prostatse")  to  inflammatory  processes. 
He  demonstrated,  referring  to  Socin  (119),  that  the 
"Prostatitis  chronica,"  which  in  general  has  been  very 
little  investigated,  is  a  chronic  catarrh  of  the  mucous  mem- 
brane, extending  from  the  mucous  membrane  of  the  ure- 
thra toward  the  interior  of  the  prostate  gland ;  and  that 
the  stroma  takes  a  part  in  severe  cases  only  of  inflamma- 
tory processes.  The  "prostatis  chronica"  might  thus  be 
regarded  as  a  "parenchymatous"  process,  while  the 
"fibroma  dififusum  prostatae"  should  be  regarded  as  a 
process  mainly  "interstitial."  Regardingthe  possibility  that 
the  "parenchymatous"  process  early  involves  the  "inter- 
stitial" tissues  and  the  view  advocated  by  many  investi- 
gators that  the  "hypertrophy"  takes  its  origin  in  the 
parenchyma,  it  is  admitted  by  Casper  himself :  "These  ob- 
jections can  hardly  be  refuted,  as  the  pathological 
anatomy  belongs  really  to  the  most  poorly  investigated 
part  of  the  pathology,  and  too  little  is  known  on  this 
point."      (1.  c.  p.  156). 

A  greater  importance  might  be  laid  to  Casper's  view  on 
account  of  the  fact  that  only  exceptionally  can  an  enlarge- 
ment of  the  prostate,  which,  however,  again  disappears,  be 
caused  by  chronic  inflammatory  processes.  "On  the  con- 
trary, as  a  product  of  the  round-cell  accumulation,  which 
is  clearly  an  inflammation,  they  have  everywhere,  as  also 
here,  a  tendency  to  contraction  on  account  of  their  trans- 
formation into  cicatricial  tissue.  In  the  hypertrophy  also 
the  latter  is  not  missing,  but  it  is  a  continually  advancing, 
ever  new,  tissue-producing  process,  from  which  finally  an 
enlargement  of  the  prostate  results."     (1.  c.  p.  157). 

These  doubts  raised  by  Casper  are  removed  by  the  pe- 
culiar structure  of  the  prostate  gland  and  the  peculiar  de- 
velopment of  its  changes,  which  have  already  been  treated 
in  the  previous  chapter. 

There  at  once  arises  the  objection  that  such  an  extensive 
connective-tissue  proliferation  as  is  sometimes  to  be  ob- 
served in  the  enlarged  prostate  gland  can  never  be  pro- 
duced by  an  inflammatory  irritation.  Leaving  aside  the 
abundant    connective-tissue    proliferations    produced    by 

128 


certain  chronically  acting  infectious  irritations  (for  in- 
stance, tuberculosis),  and  which  often  appear  directly  to 
one  as  tumors,  we  may  point  to  the  quantities  of  con- 
nective-tissue, sometimes  very  great,  which  are  formed 
during  the  course  of  a  chronic  inflammation,  or  are  the  re- 
sults of  some  acute  inflammation.  The  fibrous  thickening 
of  the  pleura,  which  sometimes  gives  rise  to  the  formation 
of  a  connective-tissue  layer  as  much  as  i  cu.  thick;  the 
so-called  organization  of  the  para  and  peris-metritic  ex- 
udates, which  may  lead  to  the  formation  of  compact  con- 
nective-tissue masses,  and  the  post-inflammatory  indura- 
tion of  some  organs,  which  sometimes  lead  not  to  a  shrink- 
age, but  on  the  contrary,  to  an  enlargement  of  the  organs 
— these  examples  may  suffice  to  show  that,  aside  from  the 
so-called  infectious  granulation  tumors,  there  exist  still 
other  post-inflammatory  processes,  which  occur  together 
with  a  connective-tissue  production  and  enlargement  of 
the  alTected  organ. 

The  changes  which  I  observed  in  the  "hypertrophy ing" 
prostate,  if  one  wishes  to  make  this  distinction,  are  to 
be  regarded  as  parenchymatous  as  well  as  interstitial.  The 
changes  in  the  glandular  epithelium,  together  with  the 
endoglandular  suppurative  processes  which  are  some- 
times encountered,  may  in  this  sense  be  designated  as 
parenchymatous,  either  catarrhal  or  catarrhal-suppura- 
tive inflammation ;  and  the  changes  in  the  stroma  may  be 
regarded  as  a  chronic  interstitial  inflammation. 

The  objection  that  the  inflammatory  processes  which  I 
observed  in  the  enlarged  prostate  glands  do  not  stand  in 
an  intimate  causative  relation  to  the  "hypertrophy,"  but 
are  an  accidental  complication,  due  to  inflammation  of  the 
neisfhboringf  orsrans,  as  for  instance  the  bladder,  I  can 
easily  dispute,  as  I  selected  for  my  investigation,  with  a 
few  exceptions,  only  such  cases  as  were  free  from  such 
complications  of  the  urinary  duct.  Finally  the  objection 
might  still  be  possible  that  the  changes  observed  by  my- 
self are  a  process  "sui  generis ;''  that  even  if  they  have  the 
characteristics  of  inflammatorv  processes,  still  they  are 
different  from  the  chronic  inflammation  of  the  prostate 
which  occur  during  middle  life.  Between  these  two  in- 
flammatorv processes  there  is  really  a  difference.  Just 
this  difference  explains  to  us  the  relatively  late  formation 
of  the  "hypertrophy"  and  its  slow  course.    The  difference, 

129 


however,  is  not  a  qualitative,  but  entirely  a  quantitative 
one.  The  inflammatory  processes  producing  the  prostate 
enlargement  show  a  ver}'  chronic,  extremely  insidious 
course ;  and  they  possess  a  relatively  insignificant  extent 
and  intensity.  For  this  reason  the  whole  process  develops 
only  step  by  step,  and  it  lasts  many  years  before  it  pro- 
duces the  symptoms  which  may  be  recognized  by  the 
clinicial.  Since  the  publication  of  the  excellent  and  ex- 
haustive investigations  of  Fenger  (148-155),  the  pre- 
viously dark  field  of  the  pathological  histology  of  chronic 
prostatitis  (aside  from  its  cause),  has  now  become  more 
clear.  From  the  detailed  description  of  the  cases  ex- 
amined by  Fenger,  and,  furthermore,  from  the  accom- 
panying illustration,  it  appears  tJ.at  the  changes  found 
by  him  produced  by  the  chronic  inflammation  of  the  pros- 
tate are  entirely  identical  zvith  those  zvhich  I  found  in  the 
enlarged  prostate  gland.  Here,  as  there,  occurs  a  ca- 
tarrh, or  a  suppurating  glandular  inflammation  ;  here,  as 
there,  subepithelial,  peri-glandular  round-cell  infiltrations 
are  to  be  observed ;  finally,  in  both  instances,  the  process 
appears  in  groups  and  irregularly,  in  that  it  appears  now 
only  in  the  gland  tubuli,  now  only  in  the  stroma,  and 
finally  in  both  in  one  and  the  same  place.  Between  Fen- 
ger's  observation  and  mine  there  exists  a  double  differ- 
ence :  First,  in  regard  to  the  extent  and  intensity  of  the 
inflammatory  processes ;  and,  secondly,  in  regard  to  their 
relative  frequency.  The  second  difference  depends,  how- 
ever, on  the  first.  The  changes  described  by  Fenger  have 
a  greater  extent  than  those  of  the  prostate  hypertrophy. 
Fenger,  for  instance,  encountered  in  his  specimens  round- 
cell  infiltrations  which  include  the  whole  extent  of  the 
vera-montanum.  In  the  stroma  of  the  prostate  the  in- 
filtrates were  more  numerous,  of  a  larger  size,  and  densely 
crowded.  In  my  specimens,  on  the  other  hand,  one  could 
hardly  encounter  two  or  three  small,  loosely  packed  in- 
filtrates in  a  section  ;  sometimes  none  were  to  be  found,  if 
the  specimen  came  from  an  unchanged  part  of  the  prostate 
gland. 

In  certain  prostate  glands  (especially  those  only  slightly 
enlarged  and  those  apparently  normal,  i.  e.,  not  enlarged), 
I  was  forced  to  explore  whole  serial  sections  to  detect  the 
changes  which  had  been  overlooked  in  a  superficial  in- 
vestigation.    In  Fenger 's  specimens  there  was  often  pres- 

130 


ent  in  the  glandular  lumina  a  pure  suppurative  contents  of 
a  contents  with  numerous  leucocytes  intermingled,  which 
seem  to  indicate  that  in  his  cases  the  cause  of  the  process 
was  quite  acute,  that  it  at  any  rate  ran  a  more  intense 
course  than  in  my  cases,  in  which  the  suppurative  contents, 
intermingling  with  the  glandular,  were  to  be  found  only 
very  rarely,  and  in  small  cjuantities,  and  that  a  pure  sup- 
purative exudate  was  the  exception.  The  importance  of 
these  dififerences  regarding  the  extent  and  intensity  of 
both  inflammatory  processes  is  obvious ;  by  it  is  explained 
the  difference  between  the  clinical  symptoms  of  both  dis- 
ease processes,  especially  the  relatively  late  occurrence  of 
the  prostate  hypertrophy.  But  they  are  also  capable  of 
explaining  ano^ther  circumstance ;  they  seem  to  indicate, 
namely,  that  the  hypertrophy  of  the  prostate  gland  must 
by  no  means  always  be  a  consequence  of  such  inflamma- 
tory processes  as  give  clinical  symptoms,  and  that  they 
are  not  always  preceded  by  anamnestic  data  zvhich  zvoitld 
prove  to  the  physician  the  diagnosis  of  prostatitis.  On 
the  contrary,  the  insignificant  extent  and  intensity  of  the 
process  which  leads  only  after  many  years  of  existence  to 
"hypertrophy"  is  so  characteristic  for  the  anatomical  pic- 
ture of  the  prostate  hypertrophy,  that  we  may  conclude 
the  absence  of  any  subjective  symptoms  at  the  beginning 
of  the  disease.  But  as  well  the  subjective  symptoms  may, 
in  consequence  of  insignificant  changes,  be  so  unimportant 
that  they  escape  the  attention  of  the  physician,  even  when 
a  special  examination  is  made  for  them.  The  ''prostate 
hypertrophy"  is  probably,  as  a  rule,  a  consequence  of 
inflammatory  processes  zvhich  are  latent  for  years  and 
produce  no  symptoms  or  very  insignificant  ones. 

In  regard  to  the  chronic  prostatitis,  "sensu  stricto,"  it 
is  generally  known  that  the  inflammatory  irritation  has 
its  point  of  origin  in  the  urinary  ducts,  especially  in  the 
urethra.  In  regard  to  the  starting-point  of  the  inflamma- 
tory irritation  producing  hypertrophy  of  the  prostate,  it 
might  perhaps  be  sought  anywhere  else — for  instance,  in 
the  blood  vessels.  However,  the  histological  changes  ob- 
served by  me  contradict  this  hypothesis.  The  inflamma- 
tory processes  following  the  course  of  the  blood  vessels 
settle  first  of  all,  according  to  experiences,  in  the  imme- 
diate neighborhood  of  the  vessels.  But  in  my  cases  there 
was  never  a  sign  of  inflammatory  changes  to  be  detected 


131 


in  the  neighborhood  of  the  vessels.  Against  this,  the 
locaHzation  of  these  changes  in  the  glands  themselves 
(endoglandular  catarrh  and  suppuration)  seems  to  argue 
that  the  inflammatory  process  has  extended  along  the 
glandular  ducts  from  the  urethra  toward  the  periphery  of 
the  prostate,  with  which  the  constant  localization  of  the 
stroma  changes  just  beneath  the  epithelium  in  complete 
harmony.  Aside  from  this,  I  found  in  the  ma- 
jority of  cases  evident  signs  of  inflammatory  changes  in 
the  urethra  in  the  form  of  subepithelial  round-cell  infil- 
tration, which  was  situated  either  in  the  vicinity  of  the 
veramontamun  or  at  other  places  of  the  mucous  mem- 
brane of  the  prostatic  urethra.  That  such  infiltrates  were 
not  found  aways  and  everywhere  in  the  urethra  is  not 
strange. 

I  have  frequently  mentioned  that  a  verv  characteristic 
symptom  of  the  inflammatory  processes  observed  by  me 
is  that  they  are  very  irregular  and  occur  onlv  in  groups. 
Besides,  the  later  stages  of  the  process,  i.  e.,  the  cicatrices, 
are  here  easily  overlooked  because  they  are  not  surrounded 
by  muscle  tissue  in  the  neighborhood  of  the  mucous  mem- 
brane of  the  urethra,  with  which  muscle  tissue  they  con- 
trast very  clearly  in  the  prostate,  and  for  this  reason  they 
are  more  easily  recognizable. 

If  we  now  question  ourselves  of  what  kind  the  inflam- 
matory process  assumed  by  us  is,  it  is  easy  to  take  it  for 
a  gonorrheal.  But  I  must  openly  confess  that  direct 
proofs  of  this  are  not  at  my  disposal. 

Such  proofs  must,  first  of  all,  be  sought  in  anamnistic 
data.  Among  several  histories  of  typical  "prostatica"^  I 
found  only  a  few  such  data  which  pointed  with  a  reason- 
able certainty  to  a  passed  gonorrhea.  In  two  patients, 
for  instance,  a  cicatricial  stricture  w^as  demonstrated  :  in 
the  posterior  of  the  urethra  in  another  was  found  a 
diffuse  narrowing  of  the  anterior  part  of  the  urethra, 
etc.  In  a  similar  situation  were  also  the  other  investi- 
g-ators  (for  inst..  Stilling  [122,  p.  21]). 

Casper  and  Jores  do  not  mention  at  all  the  course  of 
the  disease.  Only  in  the  work  of  Bohdanowicz  (7)  a 
few  cases  of  passed  gonorrheal  processes  are  specially 


^The  consent  to  examine  the  histories  I  received  from  the 
late  Prof.  Obalinsky,  and  I  wish  to  express  my  gratitude  to  Dr. 
Rutkowskl  for  his  assistance. 


133 


pointed  out :  in  other  works  they  are  entirely  absent ;  to 
which,  with  regard  to  the  previous  discussion  (p.  150  in 
MS.),  however,  not  too  much  importance  is  to  be  given. 

According  to  Neisser  and  Putzler  (120)  PezzoH  (173) 
and  GrosgHk  (159),  it  is  proved  nowadays  that  the 
gonorrheal  may  be  located  primarily  in  the  prostate  gland 
without  including  other  parts  of  the  genito-urinary  ap- 
paratus, and  that  from  the  very  first  it  may  run  a  chronic 
course.  On  the  other  hand,  it  is  to  be  seen  from  the  in- 
vestigations of  Eraud  (119)  and  Guiard  (156)  that  the 
gonorrhea  of  the  posterior  part  of  the  urethra  may  some- 
times remain  entirely  latent.  There  are  to-day  numerous 
observations,  as  those  of  Tengy,  Ghon  and  Schlagen- 
haufifer  (  147),  which  prove  that  in  the  prostate  gland  an 
inflammation  may  develop  which  is  clinically  hardly 
capable  of  diagnosis.  Through  these  facts,  the  views  ad- 
vocated by  me  and  deduced  only  from  histological  inves- 
tigation find  verification.  On  the  other  hand,  it  is  proved 
thereby  that  a  negative  anamnesis  by  no  means  argues 
against  the  gonorrheal  origin  of  the  disease.  A  further 
immediate  proof  for  the  gonorrheal  nature  of  the  "hyper- 
trophy" of  the  prostate  and  the  inflammatory  processes 
respectively  producing  it  is  to  be  sought  in  the  presence 
of  gonococci  in  the  changed  parts  of  the  prostatic  tissue. 

But  in  this  regard  my  investigations  have  furnished  no 
results.  T  was  not  able  to  demonstrate  gonococci  in  the 
parts  of  the  prostate  gland  in  cases  examined  especially 
for  it ;  consequently  an  important  factor  is  missing  to 
prove  definitely  the  relation  of  a  passed  gonorrhea  to  the 
"hypertrophy"  of  the  prostate,  but,  in  nw  opinion,  the 
possibility  of  a  relation  is  not  to  be  excluded.  I  made 
the  investigations  under  consideration  only  in  a  small 
part  of  the  cases  and  here  only  in  a  very  few  sec- 
tions. It  is,  therefore  possible  that  I  simply  overlooked 
the  gonococci-containing  tissue.  The  proof  of  the  pres- 
ence of  gonococci  in  microscopic  specimens  seems,  how- 
ever, to  be  very  difficult,  even  in  the  prostatic  inflamma- 
tion which  is  undoubtedly  gonorrheal,  as  for  a  long  time  it 
proved  to  be  a  failure.  Only  Councilman  succeeded 
("Gonorrheal  Myocarditis."  Amer.  Jour,  of  the  Med.  Sci. 
Vol.  56,  1893.  No.  3,  cit.  after  1766)  in  demonstrating 
the  presence  of  gonococci  in  the  glandular  ducts  of  the 
prostate.    Aside  from  this  author,  the  immediate  relation 


^33 


of  the  prostate  inflammation  to  the  gonorrheal  infection 
was  proved  by  von  Sehlen  (Lur  Diagnostic  and  Therapic 
der  Prostatitis  Chronica.  Centralbl.  f.  Phys,  and  Path.  d. 
Ham.  and  Sexualog.  1893.  H.  6-8,  cit.  after  1766), 
by  Neisser  and  Putzler  (170).  finally  by  Feleki  (146)1 
but  entirely  by  clinical  examinations,  since  the  gonococci 
were  found  in  the  prostatic  secretions  expressed  "per 
rectum."  Since,  therefore,  it  is  so  difficult  to  prove  the 
presence  of  gonococci  in  the  gonorrheal  prostatitis,  which 
passes  relatively  quickly  and  with  proportionally  greater 
extent  and  intensity,  it  is  not  strange  that  it  has  failed  so 
far  in  a  process  of  such  a  slow  course  and  of  such  an  in- 
significant extent  as  is  the  case  with  the  "hypertrophy"  of 
the  prostate.  Undoubtedly  certain  post-gonorrheal  proc- 
esses may  be  formed  without  the  direct  assistance  of  the 
gonococci,  and  it  is  not  impossible  that  the  prostate  "hy- 
pertrophy" also  belongs  to  these  post-gonorrheal  proc- 
esses. In  one  part  of  the  cases  of  the  chronic  urethral 
gonorrhea,  which  remains  as  a  residue  of  an  acute  in- 
flammation produced  undoubtedly  by  gonococci,  one  can- 
not by  any  means  succeed,  as  is  known,  in  proving  the 
presence  of  gonococci.  Gozzoli  (173),  for  instance,  states 
that  in  a  chronic  gonorrhea  of  the  posterior  part  of  the 
urethra  the  gonococci  are  found  in  only  eighty  per  cent, 
of  the  cases  (mostly  they  can  be  demonstrated  also  in  the 
secretion  of  the  prostate)  ;  while  the  acute  gonorrhea 
shows  the  presence  of  gonococci  in  the  full  hundred  per 
cent.  Be  this  as  it  may,  it  seems  to  be  proved  that  neither 
the  absence  of  positive  anamnestic  data  nor  the  absence  of 
gonococci  in  the  tissue  of  the  enlarged  prostate  gland_ 
argues  against  the  possibility  of  an  etiological  relation  of 
our  disease  to  the  gonorrheal  processes. 

Since  preparatory  to  this  the  immediate  proof  of  this 
relation  is  still  wanting,  the  facts  may  at  least  be  cited 
briefly  which  speak  indirectly,  with  a  certain  probability 
for  it.  First  of  all  may  be  mentioned  the  extremely  fre- 
quent occurrence  of  gonorrhea  in  man,  and  especially  the 
circumstance  that  even  at  the  beginning  of  the  disease  in 
the  acute  state  the  gonorrhea  settles  very  frequently  in 
the  posterior  part  of  the  urethra  and  the  prostate,  and 
assumes  here  very  easily  a  chronic  character.  Some 
authors  maintain  that  the  gonorrhea  attacks  very  rarely 
the  Pars  posterior  urethrse  and  the  prostate  (Jamin[i62], 

134  ;^ 


Guyon,  etc.)  ;  but  the  majority  of  the  investigators  agree 
in  the  conclusion  that  the  gonorrhea  is  very  frequent  in 
the  Pars  posterior  and  the  prostate,  respectively.  (Jadas- 
sohn, 163  [up  to  88  per  cent.]  ;  Koch,  166  [60-70  per 
cent.]  ;  Lang,  167  [80  per  cent.]  ;  Dind  [90  per  cent.]  ; 
Pezzoli,  173  [60  per  cent.]  ;  Heisler,  161 ;  Le  Provost, 
Lesser,  Rona,  Letzel  and  others.)  But,  too,  the  frequent 
inflammation  of  the  bladder  and  the  accessory  testicle  in 
gonorrhea  speaks  for  the  frequency  oi  its  localization  in 
the  posterior  part  of  the  urethra  (Aubert  [141]  and 
Eraud  [  144] )  :  finally  may  be  mentioned  the  statistics  of 
Haslund  (160),  who  found  the  involvement  of  the  deeper 
part  of  the  urethra  occurring  424  times  among  1,070  cases 
of  gonorrhea.  At  any  rate,  we  may  assume  that  in  at  least 
50  to  60  per  cent,  of  all  the  cases  of  gonorrhea  the  process 
extends  to  the  deeper  parts  of  the  urethra.  But,  according 
to  more  recent  investigations,  it  seems  to  be  above  all 
doubt  that  the  prostate  also  without  exception  suffers  at 
the  same  time.  (v.  Sehlen,  Neisser  and  Putzler,  Feleki, 
Andry  [140],  Eraud  [144],  Guiard  [156],  Neumann 
[172],  Neisser  and  Schaffer  [a76bi],  Ferger,.  Pezzoili 
[173],  Montagnon'  [163]  and  Grosglik  [159]). 

Another  circumstance  which  points  to-  the  gonorrheal 
origin  of  the  "hypertrophy"  of  the  prostate  and  certain 
forms  of  prostate  atrophy,  is  the  similarity  of  the  ana- 
tomical changes  characteristic  of  the  gonorrheal  processes 
to  those  which  we  found,  and,  furthermore,  to  certain 
complications  which  are  sometimes  observed  in  the 
gonorrhea  as  well  as  in  our  affection.  To  the  latter  oc- 
currences belong,  among  others,  the  obliteration  of  the 
"Vasa  deferentia"  observed  in  the  "hypertrophy"  of  the 
prostate;  first  pointed  out  by  Socin  (119),  and  also  by 
several  other  investigators,  which  obliteration  is  also  fre- 
quently formed  in  the  course  of  the  gonorrhea,  and  is 
proved  anatomically  by  Fenger  (150-153). 

The  common  characteristic  of  the  "hypertrophy"  of  the 
prostate  and  of  certain  consequences  of  the  gonorrhea  is, 
furthermore,  the  relatively  late  development  after  the 
gonorrheal  infection.  I  shall  mention-  especiallv  here  the 
cicatricial  post-gonorrheal  strictures  of  the  urethra.  Sta- 
tistics compiled  by  Krzysztalowicz'  embrace  121  observa- 
tions of  stricture  of  the  urethra  in  99  individuals,  of 
whom  60  acknowledged  a  passed  gonorrhea  and  5  were 

1.35 


still  suffering  from  it ;  the  most  of  those  are  between  40- 
60  years  of  age ;  in  the  greater  part  of  the  cases  the  prob- 
able symptoms  of  a  stricture  begins  after  the  50th  year. 

The  data  collected  by  Kdzystalowicz  furnish  the  proof 
that  frequently  years  pass  after  a  cured  gonorrhea  before 
the  narrowing  of  the  urethra  produced  by  the  gonorrhea 
is  felt  by  the  patient.  The  matter  is  by  no  means  different 
in  the  "hypertrophy"  of  the  prostate ;  the  period  of  the 
latent  course  of  the  disease  is  here  only  a  little  longer. 

At  this  opportunity  it  must  not  remain  unmentioned 
that,  according  to  the  investigation  of  Wassermann  and 
Halle  (176),  the  cicatricial  changes  of  the  mucous  mem- 
brane of  the  urethra  produced  by  chronic  gonorrhea  are 
by  no  means  restricted  to  the  vicinity  of  the  stricture,  but 
are  also  found  in  groups  at  many  other  places  of  the 
urethra. 

This  fact  finds  its  verification  in  the  investigation  of 
Fenger  (150-153)  ;  this  investigation  has  proved  also  that, 
although  post-g'onorrheal  strictures  are  still  unobserved  in 
the  prostatic  urethra,  this  section  is  by  no  means  free  from 
the  post-gonorrheal  cicatricial  groups.  Much  more  cer- 
tain landmarks  for  the  etiological  relation  of  the  gon- 
orrhea to  the  h3^pertrophy  of  the  prostate  gland  seem  to  be 
furnished  by  the  similarity  of  the  histological  changes  in 
both  processes.  The  characteristic  effect  of  the  gonococci 
upon  the  living  tissue  consists,  as  is  maintained  by  Fenger 
(155),  and  Teuton  (175),  in  that,  from  pus-exciting  prop- 
erties, they  have  also  the  ability  to  produce  a  proliferative 
connective-tissue  process  with  a  tendency  to  cicatricial 
shrinkage.  A  very  characteristic  symptom  in  all  proc- 
esses produced  by  the  gonococci,  according  to  the  har- 
monious statement  of  all  investigators  from  Nelson  (171), 
to  Fenger  (1.  c),  is  to  be  sought  in  the  circumstance  that 
gonorrheal  changes  progress  by  no  means  "per  continuita- 
tem,"  but  sporadically.  But  as  I  have  already  mentioned, 
inflammatory  processes  specific  to  the  "hypertrophy"  of 
the  prostate  have  the  same  characteristics  ;  and  during  the 
comparison  between  the  changes  produced  by  this  latter 
process  with  those  which  were  observed  by  Fenger  in  the 
chronic  gonorrheal  inflammations  of  the  prostate,  I  have 


^statistical  view  of  the  strictures  of  the  urethra,  which  were 
treated  in  the  surgical  division  of  the  Krakau  General  Hosp. 
in  the  years  1871-1892  (Dir.  Prof.  Obalinsky),  1893,  Polish. 

136 


already  found  opportunity  to  point  out  that  these  two 
kinds  of  changes  do  by  no  means  differ  from  each^  other 
in  a  morphological  respect,  if  we  overlook  the  quantitative 
differences.  Finally,  still  another  circumstance  may  be 
cited,  which,  although  of  no  value  as  an  indirect  proof  of 
the  etiological  importance  of  gonorrhea  in  prostate  "hyper- 
trophy," is  at  any  rate  worth  noticing.  In  the  veterinary 
literature  I  found  the  data  already  mentioned  (p.  147  in 
MS.  bot.  pge.),  from  which  it  appears  that  the  hypertrophy 
of  the  prostate  occurs  among  the  domestic  animals  only 
in  dogs.  The  only  observation  noted  in  the  literature 
within  my  reach,  of  a  cystic  degeneration  of  the  prostate 
glands  in  animals  refers  also  to  a  dog  (Csokor  [316]). 
But  from  my  investigation  it  seems  to  appear  that  the 
origin  of  cysts  in  the  human  prostate  stands  in  a  certain 
relation  to  the  changes  leading  to  a  "hypertrophy''  of  the 
organ.  In  this  regard  there  seems  to  exist  a  certain  rela- 
tion between  the  human  pathology  and  that  of  anirnals. 
Aside  from  the  balanitis  which  occurs  in  different  kinds 
of  animals  from  the  most  different  causes,  there  exists,  as 
it  seems,  a  genuine  suppurative  inflammation  of  the 
urethra,  and  again  only  in  dogs. 

(Bruckmuller  [315,  p.  675]).  Although  Moller  (320, 
p.  447),  maintains  that  such  urethritis  is  only  observedin 
male  dogs,  it  is  stated  from  other  investigators  as  for  in- 
stance Konhauser  (319,  p.  120),  and  Roll  (321,  p.  446), 
that  the  urethritis  mentioned  is  capable  of  being  trans- 
ferred from  one  animal  to  another,  which  seems,  at  any 
rate,  to  point  to  the  infectious  character  of  this  disease. 
It  would  surely  be  worth  while  to  subject  this  condition 
with  regard  to  the  similarity  to  the  human  gonorrhea  to  a 
more  exact  investigation.  According  to  Neisser  and 
Schiiffer  (176B),  all  experiments  in  cultivating  the  gono- 
coccus  in  the  organism  of  different  animals  have  been 
without  result.  The  only  real  positive  result  from  in- 
oculation was  obtained  apparently  by  Turro  (176a),  and 
again  only  in  dogs,  in  which,  by  the  effect  of  the  virulent 
gonococci  grown  upon  acid  culture-media,  a  suppurative 
inflammation  of  the  urethra  progressing  to  the  higher  parts 
of  the  urethra  was  supposed  to  be  formed. 

As  much  as  my  views  upon  the  nature  of  the  so-called 
prostate  "hypertrophy"  differ  from  the  views  at  present 
prevaihng,  still  they  are  nothing  but  a  modest  completion 


137 


of  the  following-  view  long  ago  cited  by  Virchow :  "The 
chronic  catarrh  of  the  pars  prostatica  urethrse  and  of  the 
prostate  itself,  especially  after  a  gonorrhea,  are  more  fre- 
quently the  irritating  causes  of  the  enlargement."  ("Die 
krankhaften  Geschwiilote,"  135,  p.  139). 


ETIOLOGY. 

For  the  present  we  must  limit  ourselves  to  the  following 
conclusions : 

The  foundation  for  the  "hypertrophy"  of  the  prostate 
g"land  and  certain  forms  of  prostatic  atrophy  in  my  cases 
at  least  consisted  in  chronic  inflammatory  processes,  the 
etiological  relation  of  which  to  the  virulent  g"onorrhea  is 
not  sufficiently  proved  at  the  present.  The  great  fre- 
quency of  gonorrhea  in  general,  and  especially  the  great 
frequency  of  chronic  prostatic  inflammation  even  due  to 
it  in  the  absence  of  acute  inflammations  of  the  urinary 
passages,  and  more  particularly  in  view  of  the  conspicu- 
ous similarity  of  the  observations  made  by  myself  of  the 
anatomical  data  of  gonorrheal  processes,  makes  it  possible 
that  such  a  relation  exists. 

If  the  gonorrhea  really  is  the  most  frequent  and  most 
important  cause  of  the  "hypertrophy"  of  the  prostate 
gland,  it  will  be  the  work  of  the  future  to  decide  this 
question  once  for  all. 


138 


APPENIDX 
Methods  of  Investigations 

After  the  internal  organs  were  dissected  in  the  usual 
way,  the  bladder  was  opened  "in  situ"  in  each  individual 
case  in  the  upper  part  of  the  anterior  wall.  The  state  of 
the  base  of  the  bladder  and  of  the  urethral  opening  was 
examined,  the  urine  was  drawn  and  its  quantity  measured. 
Then  the  aorta,  with  its  lateral  branches,  was  dissected,, 
and  the  extent  and  intensity  respectively  of  the  arterio- 
sclerotic changes  in  every  individual  branch  were  macro- 
scopically  considered,  and  the  renal  and  bladder  arteries, 
also  the  hypergastric  with  its  smaller  branches,  were  sub- 
jected to  a  more  special  attention  and,  if  need  required, 
parts  of  the  vessel  were  saved  for  microscopical  investiga- 
tion. 

In  addition,  the  condition  of  the  arteries  of  the  base  of 
the  brain,  of  the  extremities  and  of  the  arterial  coronariae 
cordis  was  considered  in  each  individual  case.  The  genito- 
urinary organs  were  removed  as  a  whole ;  their  anatomical 
relations  to  the  orificium  vesicale  were  exactly  noted ;  the 
prostate  gland  was  very  carefuUy'dissected  out,  measured 
and  weighed,  and  finally  divided  in  horizontal  sections 
(sometimes  after  a  sagittal  diameter),  to  judge  of  the 
state  of  the  prostatic  urethra.  For  the  microscopic  in- 
vestigation, parts  of  both  kidneys  and  of  the  bladder 
(from  the  upper,  anterior,  posterior  and  inferior  wall), 
were  cut  out,  aside  from  the  parts  taken  from  the  ar- 
teries and  from  the  prostate  glands. 

Hardening :  As  a  rule  4  per  cent,  formalin  partly  a  mix- 
ture of  sublimate  and  osmic  acid.  Hardening  in  Alcohol : 
Imbedding  in  celluloidin  stains.  Ehrlich's  Hamotoxylin,  or 
P.  Mayer's  Hamatein  (diluted  solutions  during  24  hours. 
Afterstain  :  Eosin,  orange, G).  Grenscher-Pisenti's  carmin, 


139 


Orth's  Picrolithionkarmin,  Van  Gieson's  stain,  Knhne's 
goccocci  stain. 

The  material  was  also  partly  investigated  on  frozen 
sections  treated  with  anilin  dyes  or  unstained,  as  well  as 
after  the  formalin  freezing  method  (first  worked  out  by 
Doc.  Dr.  Nowak-Krakau  and  introduced  in  1894  to  the 
Congress  of  Polish  investigators  of  natural  science  and 
physicians  in  Lemberg,  and  published  later  by  Plenge, 
Cullen  and  others). 

Each  part  of  the  bladder  wall  was  cut  in  its  longi- 
tudinal and  transverse  direction,  and  the  prostate  gland 
throughout  its  whole  right  and  left  halves  respectively  in 
a  horizontal  plane  (vertical  to  the  axis  of  the  urethra). 
After  the  removal  of  the  greater  amyloid  bodies,  such  sec- 
tions of  the  prostate  are  to  be  obtained  quite  thin,  mostly 
10-15  thick.  (The  thickness  of  the  section  is,  under  no 
condition,  by  no  means  indifferent.)  The  manner  of  the 
microscopical  investigation  was  repeatedlv  mentioned  dur- 
ing the  course  of  the  previous  treaties.  The  micro-metric 
measurements  of  every  preparation  at  10-15  places  in  a  di- 
rection vertical  to  the  bladder  wall  (parallel  with  the  di- 
am,eter  of  its  thickness),  and  10-15  arterioles,  respectively, 
of  the  bladder  wall  or  of  the  prostate,  were  made  with  the 
ocular  micrometers  with  objective  systems  2  and  8a 
(Reichert,  constant  length  of  the  tube  160  mm.).  The 
following  compilation,  taken  from  case  No.  i,  may  serve 
as  an  example : 


Vertical 

/ 

2         3 

4   1    J   1    6 

7 

8       q\  10 

A  vei-age 

Anterior 

Con.  tissue 

1615 

I  SIC 

'785 

1275 

850  1530 

1700 

1360 

1 

I 105  1360 

1 400-1 

.4  mm. 

Blad.  wall 

Musculature 

40S0 

493° 

2040 

240  S 

3^30 

30D0 

3230 

2720 

3400  4250 

3309-3 

.3  mm. 

Upper 

Con.  tissue 

76s 

1105 

Q2S 

IS^o 

1360 

1020 

1360 

850 

1360 

1 105 

1 1 59 

Wall 

Musculature 

28QU 

2210 

22qs 

^82S 

3060 

28Q0 

2550 

3400 

2380 

3060 

2856 

Posterior 

Con.  tissue 

lies 

76^ 

76s 

8  SO 

765 

1020 

850 

7D5 

705 

850 

850 

Wall 

Musculature 

2720 

2040 

2125 

2040 

2210 

2550 

2210 

2210 

2040 

2125 

2227 

Base  of 

Con .  tissue 

1020 

1020 

1020 

1105 

8so 

92  s 

1020 

1 190 

850 

1020 

1003 

Bladder 

Musculature 

2S90 

2805 

2805 

297  s 

2465 

289c 

2890 

2720 

3060 

2380 

27SS 

Measurements  executed  with  oc.  3  obj.  3  Reichert  (160  mm.    length   of    tlie  tube).     The 
relative  proportions  calculated  from  the  average  numbers 

Anterior  wall  Upper  wall  Posterior  wall  Base  of  blad. 
Connect,  tissue  :  Musculature—         1:2.37  1:2.5  1:2.62  1:2.77 

For  histological  material  I  had  at  my  disposal  over 
3,500  slides  (not  counting  the  frozen  sections  and  the 
formalin  frozen  section).  For  examining  the  prostate 
sections  for  the  making  of  the  drawing  I  used  Leiss'  Ap- 


140 


pochromate  (Leiss  lamera  lucida?  [Zeichenkammer]  ). 

In  consideration  of  the  circumstances  that  in  the  coin^se 
of  the  previous  treaties  all  the  investigated  cases  were 
compiled  in  several  Tables,  and  that  the  more  important 
cases  were  furthermore  particularly  discussed  in  the 
proper  places,  I  think,  contrary  to  my  original  intention, 
it  is  not  necessary  to  add  to  the  treaties  a  detailed  descrip- 
tion of  the  cases  examined.  Better  to  illustrate  the  man- 
ner of  the  investigation  in  individual  cases.  I  cite  here  as 
an  example  one  case  (i)  Wl.  Carl,  69  years  old  (clinical 
diagnosis:     Arteriosclerosis). 

Section  diagnosis  (Nov.  12,  1895).  Haemorrhagia 
cerebelli  atheroma  arteriarum.  Hypertrophic  cordis  sin- 
istri.  Atrophia  renum  senilis  cystitis  v  pyelitis  catar- 
rhalis. 

General  Nutrition  :  Fair.  I.  Macroscopical  investiga- 
tion (a)  arterial  system;  i,  thoracis  and  abdominal  aorta; 
2,  a  common  iliac ;  3,  hypogastric  atheroma,  decreasing  in 
intensity  toward  the  periphry ;  4,  vesical  arteries ;  5,  pros- 
tatic arteries ;  6,  renal  arteries ;  wall  thin,  intima  smooth. 
Atheroma  of  the  arteries  at  the  base  of  the  brain  and  the 
extremities  (b)  i,  kidneys  simple  senile  artrophy  with 
catarrhal  pyelitis  (for  want  of  space  the  schematic  de- 
scription was  referred  to  the  text  of  the  work)  ;  2,  bladder 
contains  580  c.cm.  turbid  urine^  mucous  membrane 
slightly  injected  lusterless,  at  places  slate-colored,  here 
and  there  hemorrhagic  spots,  numerous  large  muscular 
ridges,  no  diverticuli.  The  base  of  the  bladder  behind 
the  prostate  pathologically  deepened. 

Posterior  lip  of  the  orificium  projects  forward  in  the 
form  of  a  transverse  mound.  To  the  right  a  polypoid  tu- 
mor of  half  the  size  of  a  hazelnut.  Orificium  itself  de- 
formed, forming  an  irregular  crescesitic  opening  pointed 
with  the  convexity  to  the  left.  3.  Prostate  gland  en- 
larged of  increased  consistency ;  the  right  lateral  lobe 
much  larger  than  the  left,  a  left  lateral  deviation 
of  the  prostatic  urethra,  in  addition  a  strong  deviation  to- 
ward the  posterior.  The  right  projection  at  the  orificium 
mentioned  proves  to  be  a  part  of  the  enlarged  right  pros- 
tate lobe.  In  the  cross-section  of  the  prostate  numerous  tu- 
mors project,  especially  on  the  right  side  (pseutoadeno- 
mata),  which  have  in  places  a  delicate  cavernous  struc- 
ture.    Weight  of  the  prostate  31.2  grams.     Length  (from 

141 


basis  to  apex),  4.5  cm.  Greatest  width  (at  the  base), 
3.9  cm.  Greatest  thickness,  3.4  cm. ;  4,  urethra  outside  of 
the  prostatic  part  otherwise  unchanged. 

II.     Adicroscopic  Examination. 

a.  Arteries.  In  the  |  fnal,  vesical  and  prostatic  arteries 
outside  of  the  organs  nf  sign  of  atheromatosis  is  to  be  de- 
tected, the  arterioles  of-  the  bladder  wall  and  of  the  pros- 
tate unchanged.  The  relative,  numerical  proportions 
calculated  by  micrometic  measurement  (made  in  the  way 
mentioned). 

Anterior  wall  Upper  wall  Posterior  wall  Base  of  bladder 
Intima  i  i  i  i 


3  =  2.7  =. 


Adventitia  2.5  2.0  2.S  2.8 

Seemen  i  i  i  i 

Wall  0.4  0-39  0-34  0.41 

b.  Genito-urinary  apparatus,  i,  Kidneys:  The  micro- 
scopical picture  corresponds  on  the  whole  to  the  simple 
senile  atrophy ;  ( for  want  of  space  the  schematic  de- 
scription was  referred  to  the  text  of  the  work).  2.  Blad- 
der. The  thickness  of  the  wall,  leaving  out  the  subserous 
tissue,  is  44—5  mm.  at  the  upper  and  anterior  wall,  at  the 
base  of  the  bladder  3^-4  mm.,  at  the  posterior  wall  4  mm. 
The  mucous  membranes  moderately  thrown  into  folds, 
epithetum  missing  nearlv  everywhere,  here  and  there  small 
and  loose  round-cell  infiltrates.  The  submucosa  is  broad, 
composed  of  quite  loose  tissue;  here  and  there  sparingly 
loose,  round-cell  infiltrates,  situated  mainly  in  the  neigh- 
borhood of  the  dilated  vessel  filled  with  blood  corpuscles. 
At  the  upper  wall  (in  the  vicinity  of  the  apex  of  the  blad- 
der), extensive  extravasations  within  the  reach  of  the 
submucosa.  The  bladder  muscle  forms  two  layers  in  the 
vicinity  of  the  anterior  wall  and  base  of  the  bladder,  which 
layers  are  mainly  to  be  differentiated  by  the  different  di- 
rection of  the  courses  of  the  muscle  bundles,  as  they  are 
not  limited  by  any  connective-tissue  layer  worth  men- 
tioning. 

The  thickness  of  both  layers  is  very  variable  in  dif- 
ferent places,  but  as  a  whole  the  external  layer  is  broader 
than  the  internal.  To  these  two  layers  is  added  a  third  in 
the  posterior  wall  which  lies  mnermost,  and  is  distributed 
irregularly  (it  forms  net-like  trabeculae  running  in  dif- 
ferent directions)  ;  this  layer  is  much  narrower  than  the 
other  two.     In  the  neighborhood  of  these  three  layers  in 


142 


the  posterior  wall,  one  is  able  to  distinguish  several 
smaller  layers  of  the  second  class.  In  the  neighborhood 
o£  the  apex  of  the  bladder  no  clear  regularity  can  be 
demonstrated  in  the  distribution  ^f  the  muscle  tissue ;  here 
exist  several  small  layers  inter]  ced  with  each  other  in 
different  directions  and  of  diffe  -ent  and  variable  thick- 
ness. The  peri  and  inter-itiuscular  connective-tissue 
framework  is  quite  scarce  and  as  a  whole  loosely  formed. 
The  perivascular  and  interfascicular  connective-tissue 
septa  [ziige?]  are  of  equal  width,  with  the  exception  of  the 
latter  in  the  neighborhood  of  the  most  external  muscular 
layer  of  the  anterior  wall.  Here  they  are  broader  than  the 
connective  tissue  septa  [ziige]  which  separate  the  two 
muscular  layers  from  each  other.  With  weaker  lenses 
(Reichert  3"  III.),  the  interfibrillar  connective-tissue  is 
visible  only  on  the  transverse  section  of  the  muscle 
bundles,  and  only  in  the  neighborhood  of  the  apex  and 
base  of  the  bladder.  In  sections  of  the  anterior  and  pos- 
terior wall  nothing  can  be  seen  with  this  lens.  The  sub- 
serous connective-tissue  most  external  to  the  bladder  wall 
is  scarce  and  loosely  joined,  the  fat  tissue  insulas  are  pres- 
ent only  here  and  there  in  its  vicinity,  nowhere  joined  out- 
side it,  i.  e.,  between  the  muscle  bundles.  The  relative 
proportions  of  the  components  of  the  bladder  wall  cal- 
culated by  micrometric  measurements : 

Anterior  wall  Upper  wall  Posterior  wall  Base  of  bladder 

Connective-tissue  _  i  _  i  _  J  _        ^ 

Musculation  ~  2.37  2-5  3-"^  2.77 

3.  Prostate  Gland.  In  the  section  made  horizontal  to 
the  level  of  the  vera  montamum  containing  the  entire  right 
lateral  half  of  the  prostate,  numerous  "pseudo-adenomata" 
show  the  largest  of  which  bulges  with  its  internal  circum- 
ference into  the  lateral  wall  of  the  urethra. 

Externally,  as  regards  the  pseudo-adenomata  excretory 
ducts  bent  more  sharply  than  is  normal.  At  the  periphery 
of  the  specimen  smaller  and,  as  a  whole,  unchanged  gland- 
ular branches  with  a  normal  stroma. 

The  pseudo-adenomata  are  composed  of  numerous 
glandular  acini,  dilated  in  different  degrees,  in  which  the 
epithelium  is  now  flattened,  now  missing  in  places  or  en- 
tirelv,  and  the  contents  of  which  consists  of  desquamated 
epithelial  cells,  amyloid  bodies  and  a  few  leucocytes.  The 
microscopical  picture  is  very  varied.      (On  account  of  lack 

14.3 


of  space  the  reader  is  referred  for  the  details  to  the  text 
of  the  work).  In  some  dilated  glandular  acini  the  con- 
tents consists  of  a  homog-eneous  amorphous  mass.  (Table 
XL,  Fig-,  ly).  In  the  stroma  of  the  pseudo-adenomata  the 
muscular  elements  are  mostly  missing,  while  very  com- 
pact cicatricial-like  or  new  connective-tissue  appears,  com- 
posed of  densely  packed  spindle-cells.  Here  and  there 
subepithelial  round-cell  infiltrates  and  subepithelial  ring- 
formed  cicatricial  groups  narrowing  the  lumen  of  the 
glandular  ducts.  (For  details  see  text  v/ork).  The 
changes  in  the  stroma  are,  as  a  whole,  not  particularly 
numerous ;  the  clearest  changes  lie  in  the  neighborhood  of 
the  distal  ends  of  the  main  excretory  ducts  of  the  right 
lateral  lobe  at  the  external  border  of  the  largest  pseudo- 
adenomata  near  the  proximal  end,  i.  c,  the  termination 
of  main  ducts  narrowed  throughout,  the  neighboring 
stroma  is  composed  exclusively  of  cicatricial  tissue,  which 
forms  a  broad  band ;  this  band  lies  on  both  sides  of  the 
duct. 

In  the  left  lateral  lobe  similar  changes,  with  the  dif- 
ference that  the  pseudo-adenomata  are  smaller  and  more 
scarce  and  that  the  transitional  pictures  between  the 
pseudo-adenomata  and  the  more  or  less  normal  tissue 
parts  are  more  easily  to  be  found.  A  hard  pseudo- 
adenoma  lying  at  the  distal  end  of  the  main  duct  corres- 
ponds to  the  connective-tissue  type  described  on  p.  iii 
(in  ms.),  otherwise  the  nodules  are  composed  of  cystic- 
ally-dilated,  glandular  acini  with  thin  septae.  The  pro- 
jecting tumor  at  the  right  side  of  the  orificium  vesicale 
was  divided  in  connection  with  the  neighboring  part  of 
the  right  prostate  lobe  in  an  entire  section  series  in  a 
sagittal,  vertical  plane. 

By  this  it  will  be  shown  that  the  tumor  lies  internally  to 
the  triangular  vertical  section  of  the  sphincter,  i.  e.,  in  the 
center  of  the  muscular  ring ;  this  tumor  consists  entirely  of 
glandular  tissue,  which  is  in  connection  with  the  glandular 
tissue  of  the  upper  part  of  the  right  prostate  lobe,  and 
unites  with  the  glandular  tissue  at  the  external  side  of 
the  muscle  below  the  inferior  edge  of  the  sphincter.  The 
muscle  tissue  of  the  sphincter  is  sharply  united  everywhere 
with  glandular  tissue ;  its  wedge-shaped  transverse  section 
blunt.  The  top  of  the  tumor  consists  of  very  dilated 
glandular  acini,  with  a  mixed  contents,  and  of  relatively 

144 


broad  septae  composed  of  abundant  spindle-cell  tissue. 
Below  the  top  of  the  tumor  the  space  between  the  lumen 
of  the  urethra  and  the  sphincter  is  occupied  by  a  sing-le 
cyst  measuring-  5x3  mm. ;  in  it  the  same  homogeneous 
mass,  epithelium  extremely  flattened.  In  the  stroma  around 
the  cyst  big,  dense,  subepithelial,  round-cell  infiltrates, 
mostly  in  streaks.  Below  this  big  syst  highly  dilated 
glandular  acini  filled  with  a  mixed  contents  and  few 
(jedoch)    pseudo-adenomata. 

At  the  posterior  lip  of  the  orificium  (entire  serial  sec- 
tion), the  sphincter  lies  immediately  beneath  the  mucous 
membrane ;  between  the  sphincter  and  the  vasa-deferentia 
(i.  e.,  the  posterior  commissure  proper),  greatly  dilated 
glandular  acini  a  few  small  pseudo-ademonata,  etc.  The 
anterior  border  of  the  horizontal  section  of  the  sphincter 
bulges  forward  in  the  upper  part  (macroscopical,  visible, 
transverse  tumors  of  the  posterior  lip  of  the  orificium). 
4.  Vasa  deferentia  outside  of  the  prostate  unchanged. 


M5 


BiPLIEQi^APHY. 


A.  Bladder 

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x6     Casper,  L.,  Zur  Pathologie  des  Tractus  urogenitalis  senilis. 

146 


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24  Idem,  Ueber  Enuresis.  Wien.  med.  Jahrb.,  1872,  p.  123; 
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569- 

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37  Fenwick,  E.   H.,  The  etiology  of  prostatic  enlargements 


147 


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57  Hahn,  SiEGFR. ,  Ueber  die  verschiedenen  Leiden  der  Prostata. 
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58  Harrison,  Reg.,  The  prostate  muscle.  Lancet,  1886,  Dec. 
4,  p.  438.     VH.  II  260. 

59  Idem,  The  fibromatous  prostate.     Brit.  med.  Journ.,  1889, 


148 


p    126.     VH.  II  338. 

60  Idem,  On  the  causation  and  nature  of  hypertrophy  of  the 
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61  Home,  E.,  Pract.  observ.  on  the  treatment  of  the  diseases 
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HuETER  vergl.  Handbucher. 

62  Jean,  A.,  De  la  retention  incomplete  d'urine  dans  Ics  cas 
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63  IvERSEN,  Prostatas  normale  Anatomi.  Nord.  med.  arkiv, 
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64  Idem,  Hypertrophia  prostatae,  monografisk  fremstillet. 
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6s  JuRiE,  Beitrage  zur  Kenntnis  des  Baues  und  der  Verncht- 
ung  der  Blase  und  der  Harnrohre.  Wien.  med.  Jahrb., 
1873,  Heft  2,  p.  415—437-     VH.  I  IS  u-  65. 

66  Idem,  Ueber  die  Muskulatur  der  Harnblase.  Wien.  med. 
Wochenschr.,  1873,  No.  21. 

67  Idem,  Ueber  den  Mechanismus  der  Harnverhaltung  bei 
Greisen.  Arch.  f.  klin.  Chir.,  Bd.  21,  1877,  p.  724.  VH. 
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68  JoRES,  L.,  Ueber  die  Hypertrophic  des  sogenannten  mittle- 
ren  Lappens  der  Prostata.  Virchow's  Arch.,  Bd.  135, 
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KoNiG  siehe  Maas. 

69  KucHLER,  Ueber  Prostatavergroszerungen.  Dtsch.  Klinik, 
Bd.  50,  1866,  cf.  119. 

70  KuMMEL,  Ueber  die  operative  Bedhandlung  der  Prosta- 
tahypertrophie.  Therap.  Monatsh.,  Bd.  9,  1895,  Heft  7, 
p.  371;    Berl.  Klinik,  1895,  No.  86. 

71  KoLLiKER,  Zeitschr.  f.  wiss.  Zool.,  Bd.  i,  1849,  Heft  i,  p. 
67,  cf,  119,  loi  u.  135. 

71a  Lesine,  p.  (Recherches  expenmentales  sur  les  modifaca- 
tions  de  la  prostate  produites  par  la  castration  chez  les 
animaux.  Med.  Obozrenije,  XLVI.  14)  Ref-  Sem.  med. 
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72  Launois,  De  I'appareil  urinaire  des  vieillards  (etude  anat., 
path,  et  clin.).     These  Paris,  1885. 

73  Idem,  De  I'atrophie  de  la  prostate.  De  la  castration  dans 
1 'hypertrophic  de  la  prostate.  Ann.  des  mal.  des  org. 
gen.-urin.,  1894,  No.  10,  p.  721. 

74  Langerhans,  Ueber  die  accessorischen  Drusen  der  Ge- 
schlechtsorgane.  Virchow's  Arch.,  Bd.  61,  1874,  p.  208 
—228.  ,    ,. 

75  LuscHKA,  Das  vordere  Mittelstuck  der  Prostata  und  die 
Aberration  desselben.     Ibid.,  Bd.  34,  1865,  p.  592 — 597- 

76  Le  Dentu,  Des  vices  de  conformation  du  testicule.  These 
agreg.      Paris   1869,  cf.   73. 

77  Lubarsch,  Ueber  Cysten  der  ableitenden  Hamwege.    Arch. 


149 


f.  Mikr.  Anat.,  Bd.  41,  1S93,  p.  303. 

78  Limbeck,  Zur  Kenntnis  dcr  Epilh.  Icyslen  dcr  Harnblase 
und  dcr  Ureteren.     Zcitschr.  f.  Hcilk.,  Bd.  8,  1887,  cf.  2. 

79  Latis,  M.  R.,  Ricerche  sperimentali  riguardanti  gli  effetti 
delle  operazioni  suUa  prostata.  Riforrna  med.,  1893,  2. 
Genn.     VH.  II  327. 

80  Lydston,  J.  F.,  The  etiology  of  prostatic  hypertrophy. 
Philad.  Rep.,  1893,  May  13.     VH.  II  328. 

81  Legueu,  F.,  Des  rapports  entre  Ics  testicules  et  la  prostate. 
Arch,  de  physiol.  norm,  et  pathol.,  ser.  5,  Tome  9,  1896,  No. 

i>  P-    154—158- 

82  Lr  Roy,  Tumeur  enorme  de  la  prostate.  Prog,  med.,  1886, 
No.  17.     VH.  II  260. 

83  Le  Dentu,  Kyste  de  la  prostate.  Bull,  et  Mem.  de  la  Soc. 
de  Chir.,  Tome  5,  1879,  No.  5,  p.  27.      VH.  II  223. 

84  Maas,  Die  Krankhciten  der  mannlichen  Ham-  und  Ge- 
schleehtsorgane,  in  Konig's  Lehrbuch  der  specie  Hen  Chirur- 
gie,  Bd.  2,  1881,  3.  Aufl.,  p.  439 — 607. 

85  Mendelssohn,  Klinik  der  Krankheiten  der  Harnblase  und 
Prostata  naeh  den  Vorlcsungen  von  Prof.  F.  Guyon  bear- 
beitet  von  Mendelssohn,  1893. 

86  Misiewicz,  Nowoczesne  poglady  szkoly  Neckerowskicj  na 
tzw.  prostatyzm.  Nowiny  lekarskie,  1S95,  ^o-  2,  p.  50 
(polnisch) . 

87  MiQUET,  A.,  L'apparcil  urinaire  chez  I'adulte  et  chez  les 
vieillards.     These  Paris,  1894. 

88  MoNOD  et  Terillon,  Traite  des  maladies  du  testicule. 
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89  Idem  et  Arthaud,  Contribtition  a  I'etude  des  alterations  du 
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89a  MoTZ,  B.,  O  przeroscie  gruczolukrokowego.  Gaz.  lek.,  1895, 
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896  Idem,  Przyczynek  do  nauki  o  budowie  histologieznej 
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8gc  Mac  Ewan,  D.,  Die  operative  Behandlung  der  Prostata- 
hypertrophic.     Wien.  med.  Presse,  1897,  No.  24 — 27. 

90  Monod,  Hypertrophic  de  la  levre  postericur  du  col  de  la 
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91  Idem,  Hjrpertrophie  de  la  prostate.  Saillie  enorme  du  lobe 
moyen  etc.      Ibid.     VH.  II  232. 

92  Mercier,  A.,  Rech.  sur  les  mal.  des  org.  urin.  et  gen.,  Paris 
1 84 1. — Rech.  sur  le  traitem.  des  malad.  des  org.  urin. 
Paris  1856. — -Memoire  sur  la  veritable  cause  et  le  mecan- 
isme  de  I'incontinence,  de  la  retention  et  du  regorg':ment 
de  I'urine  chez  les  vieillards.  Gaz.  med.  de  Paris,  1840,  cf. 
119. — Memoire  sur  une  saillie  particuliere  de  la  valvule 
vesico-urethrale.  Examinat.  med.,  1841,  cf.  in. — Rcchcr- 
ches  sur  les  valvules  du  col  de  la  vessie.  2.  ed.,  1848,  cf. 
72. — Recherches  anatomiques  sur  la  prostate  d'S  vieillards. 
Gaz.  med,  de  Paris,  1S40,  p.  339,  cf.  310. — Recherches  sur  la 


nature  et  le  traitement  d'une  cause  frequente  et  peu  connu 
de  retention  d'urine.      1844,  cf.  57. 

93  MouLLiN,  C.  Mansell,  The  pathology  of  enlargement  of  the 
Prostate.      Lancet,   1894,  Vol.   2.  No.   16,  p.  908.     VH.  94 

II  537- 

94  Messer,  J.  CocKBURN,  Report  of  the  condition  of  the  prost. 
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95  MoRGAGNi,  De  sedibus  et  causis  morborum.  Epistol,  41 — 
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96  MiHALKovics,  Entwickelung  der  Harn-  und  Geschlechtsor- 
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97  Mendelssohn,  Einige  Anschauungen  Guyon's  uber  die 
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98  Obalinski,  Wyklady  z  zakresu  chorob  drog  moczowych 
meskich.      Krakow,  1886,  p.  65,  123,  131,  179,  187  (polnisch) 

99  Obersteiner,  Die  Harnblase  und  die  Uretheren,  in 
Stricker's  Handbuch  der  Lehre  von  den  Geweben,  XXIII, 
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100  Oberdieck,  H.,  Epithel  und  Drusen  der  Harnblase  und 
Harnrohre.      Gottingen  1884,  cf.  2,  171. 

loi  Pauli,  Ueber  die  Hypertrophic  der  Prostata.  Virchow's 
A  rch.,  Bd.  27,  1863,  p.  27. 

102  PosNER,  Ueber  Prostatakonkretionen.  Zeitschr.  f.  klin. 
Med.,  Bd.  16,  1889. 

103  Pelikan,  Skopzenthum  in  Ruszland.      1875,  p.  99. 

104  Paneth,  Ueber  das  Epithel  der  Harnblase.  Silzungsber. 
d.  kgl.  Akad.  d.  Wissensch.  in  Wien,  Bd.  74,  1876. 

105  PoppERT,  Zur  Kasuistik  der  Blasenhalsklappen.  Arch.  f. 
klin.  Chir.,  Bd.  44,  1892,  p.  52. 

106  PiTHA,  Krankheiten  der  mannlichen  Genitalien  und  der 
Harnblase,  in  Virchow's  Handb.  d.  spec.  Pathol,  u.  Ther., 
Bd.  6,  1856— 1865,  2.  Teil. 

io6a  Pasteau,  Trois  cas  de  prostatisme  vesical.  Ann.  des  mal. 
des  orig.  gen.-urin.,  1897,  No.  i. 

107  Przewalski,  Centralbl.  f.  Chir     1896,  No.  i. 

108  QuAiN,  R.,  Clinical  observation  on  some  forms  of  enlarge- 
ment of  the  prostate  gland  in  connection  with  diseases  of 
the  urinary  organes.  Med.  Times  and  Gaz.,  1872.  VH. 
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109  RoBELiN,  Etude  sur  les  vessies  a  cellules.  Paris  1886. 
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no  Robin  et  Cadiat,  Sur  la  structure  intime  de  la  muqueuse 
et  les  glandes  tu-ethrales  de  I'homme  et  de  la  femme. 
Joum.  de  I'anat.  et  de  la  physiol.,  1874,  p.  514,  nach  40. 

111  Rudinger,  Zur  Anatomie  der  Prostata  etc.  Festschr.  d. 
arztl.  Ver.  Munchcn,  1883,  cf.  68. 

112  RoKiTANSKY,  Lchrbuch  der  pathologischen  Anatomie,  Bd. 
3,   1 86 1,  p.  368. 

113  Reichel,  Die  Entwickelung  der  Harnblase  und  Harnrohre. 


Verhandl.  d.  Wurzburger  med.-phys.  Gcsellsch.,  N.  F.,  Bd. 
27,  1893,  cf.  2. 

114  Regnault,  Etude  sur  revolution  de  la  prostate  chez  le 
chien  et  chez  I'homme.  Journ.  de  I'anat.,  T.  28,  1892, 
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115  Reinert,  Ueber  Ganglienzellen  der  Prostata.  Zeitschr.  f. 
ration.  Med.  Bd.  34,  p.  194,  cf.  119. 

116  Recamier,  Atherome  arteriel.  Prostatisme  chez  un 
homme  jeune.  Ann.  des  nial.  des  org.  gen.-urin.,  1889, 
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117  Sappey,  Traite  d'anatomie  descriptive.  Tome  4,  1879, 
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118  Strauch,  Ph.,  Ein  Beitrag  zur  Kasuistik  der  Prostataa- 
trophie.  Centralblatt  f .  d.  Krankh.  d.  Harn-  u.  Sexualorg. 
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119  SociN,  Krankheiten  der  Prostata,  in  Pitha-Billroth, 
Handbuch  der  Chirurgie,  1871 — 1875,  Bd.  3,  Abt.  2,  Heft 
8,  2.  Halfte. 

120  Stilling,  Beobachtungen  uber  die  Funktion  der  Prostata 
und  uber  die  Entstehung  der  prostatischen  Konkremente. 
ViRCHOw's  Archiv,  Bd.  98,  1884,  Heft  i,  p.  i — 21. 

121  ScHUH,  Hypertrophic  der  Vorsteherdruse .  Oesterr. 
Zeitschr.  f.  prakt.  Heilkd.,  1855,  Gesamm.  Abhdl.,  p.  436, 

cf.  119.  57- 

122  SvETLiN,  W.,  Einige  Bemerkungen  zur  Anatomic  der 
Prostata.  Sitzungsberichte  d.  Wien.  Akad.  d.  Wissensch., 
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123  ScHLANGE,  Ueber  Prostatahypertrophie.  Arch.  f.  klin. 
Chir.,  Bd.  87,  1888,  p.  769.      VH.  II  333,  cf.  310. 

124  Salvioli,  Contribuzione  alio  studio  degli  adenomi.  Gaz. 
dclla  clin.  di  Torino,  1876,  nach  72. 

125  Stockton-Hough,  J.,  A  new  theory  concerning  the  proxi- 
mate cause  of  the  enlargeinent  of  the  prostate  body  (gland) 
Philad.  med.  Times,  1874,  Febr.     VH.  II  297. 

126  Santesson,  C,  og  Key,  A.,  Myoma  adenomatosum  pros- 
tatae.      Nordiskt  med.  Arkiv.,  Bd.  2,  No.  27.     VH.  70  II 

791- 

127  TouRNEAUX,  Sur  le  developpement  et  revolution  du 
tuberc.  genit.  chez  le  foetus  humain  avcc  remarques  con- 
cern, le  developpement  des  glandes  prostatiques.  Journ. 
de  I'anat.  et  de  la  phys.,  Tome  25,  1889,  p.  229,  cf.  2. 

128  Tillmann's  Lehrbuch  der  Chirurgie.  Leipzig  1892,  2. 
Aufi.,  Bd.  2,  Tcil  2,  p.  249.  362. 

129  TuFFiER,  Du  role  de  la  congestion  dans  les  maladies  des 
voies  urinaires.  These  1885.  Ann.  des  mal.  des  org. 
gen.-urin.,  1886,  p.  436.     VH.  II  239. 

130  Thompson,  H.,  The  enlarged  prostate,  its  pathologj-^  and 
treatment.  Lcndon  1858,  cf.  Transact,  of  the  pathol. 
Soc,  Vol.  9,  p.  298,  cf.  119,  136 — Some  observat.  on  the 
anatomy  and  pathology  of  the  adult  prostate.  Med. -chir. 
Trans.,  Vol.  40,  1857,  cf.  119. — Rare  form  of  enlargement 
of  the  prostate.      Lancet,  1857,  V^l.  2,  p.  24,  cf.  119. 

131  Thompson,  H.,  On  the  nature  of  the  so-called  hypertrophy 


152 


of  the  prostate.      Brit.  med.  Joum.,  1886,  Vol.  i,  p.  1156. 
VH.  II  260. 

132  Idem,  The  diseases  of  the  Prostata,  Ed.  6,  1886.  VH. 
II  260. 

133  Idem,  Die  chirurgischen  Krankheiten  der  Harnorgane. 
Autoris.  dtsch.  Ausg.  v.  Dupuis.  Nach  der  4.  Aufl.  des 
Orig.  BerHn  1877. — Die  Krankheiten  der  Harnwege. 
Nach  der  8.  Aufl.  des  Orig.  ubersetzt  u.  mit  Rucksicht  auf 
die  deutsche  Litteratur  bearb.  von  L.  Casper,  Munchen 
1889. 

134  ViRCHOw,  Ueber  die  Prostatakonkretionen  beim  Weibe. 
ViRCHOw's  Arch.,  Bd.  5. 

135  Idem,  Die  krankhaften  Geschwulste,  Bd.  3,  1863,  Abt.  i, 

P-   133—139-  ' 

136  Wyss,  Die  heterologen  Neubildungen  der  Vorsteherdruse. 
ViRCHOw's  Arch.,  Bd.  35. 

137  Zambianchi,  Contribution  a  I'etude  de  1 'hypertrophic  de 
la  prostate.     These.      Paris  1875,  cf.  72,  87,  40. 

138  White,  J.  W.,  The  present  position  of  the  surgery  of  the 
hypertrophied  prostate.  Trans,  of  the  Amer.  Surg.- 
Assoc,  Vol.  II,  p.  167;  Brit.  med.  Journ.,  1893,  Sept.  9, 
p.  575.     VH.  II  328. 

139  Wilson,  Alb.,  The  mechanisme  of  prostatic  obstruction 
illustrated  by  a  case  of  vesical  tumour.  Edinb.  Journ., 
1890,  p.   1021     VH.    II     308. 

B.  Gonorrhea 

140  Andry,  Precis  des  maladies  blennorrhagiques,  1894. 

141  AuBERT,  P.,  Sur  I'etat  latent  du  debut  de  la  cystite  blen- 
norrihagique.      Lyon  med.,  1884,  No.  24.     VH.  II  224. 

142  Cooper,  A.,  Chronic  prostatitis.  Brit.  med.  Journ.,  1887, 
p.  327.     VH.  II  312. 

143  Deniam,  Essai  sur  1 'inflammation  subaigue  de  la  prostate 
chez  les  adultes.      Paris  1865,  cf.  119. 

144  Eraud,  J.,  De  I'urethrite  posterieure  simple  ou  compliquee. 
Lyon  med.,  1885,  No.  4  u.  5.     VH.  II  238. 

145  Priedlander,  Ueber  die  chronische  Gonorrhoe  des  Mannes 
und  ihre  Hcilbarkeit.  Dermatolog.  Zeitschr.,  Bd.  i,  1893 
— 1894.     VH.   1894,   II   704. 

146  Feleki,  Beitrage  zur  Kenntnis  und  Therapie  der  chronis- 
chen  Entzundung  der  Prostata  und  Samenblaschen. 
Centralbl.  f.  d.  Krankh.  d.  Ham-  u.  Sexualorg.,  1895, 
Heft  9  u.  10. 

147  Finger,  E.,  Ghon  und  Schlagenhaufer,  Beitrage  zur 
Biologic  des  Gonococcus  und  zur  pathologischen  Anatomic 
des  gonorrhoischen  Prozesses.  Arch.  f.  Dermatol,  u. 
Syphil.,  Bd.  28,  Heft  i  u.  2. — Weiterer  Beitrag  ibid.,  Bd. 

?,5  P-   141- 

148  Finger,  E.,  Wien.  med.  Wochenschr.,  1890,  No.  2 — 4. 

149  Finger,  F.,  Beitrage  zur  pathologischen  Anatomic  der 
chronischen  Urethritis  posterior  und  der  chronischen 
Prostatitis  blennorrhagica.      Verdandl.  d.  2.  internal,  der- 


153 


matol.  Kongr.  in  Wien,  1892.      Wien  1893,  p.  748 — 754. 

150  Idem,  Beitrage  zur  pathologischen  Anatomie  der  Blen- 
norrhoe  der  mannlichen  Sexualorgane.  I.  Die  chronische 
Urethralblennorrhoe.  Arch.  f.  Dennat.  u.  Syph.,  1891, 
Erganzungsheft  i,  p.   i — 55. 

151  Idem,  Beitrage  zur  pathologischen  Anatomie  der  Blen- 
norrhoe  der  mannlichen  Sexualorgane.  II.  Die  chronische 
Urethritis  posterior  und  die  chronische  Prostatis.  Ibid., 
1893,  Heft  I,  p.  27 — 69. 

152  Idem,  Zur  pathologischen  Anatomie  und  Klinik  der 
Prostatitis  blennorrhagica  acuta.  Allgem.  Wiener  med. 
Ztg.,  1893,  No.  7 — 8. — Zur  pathologischen  Anatomie  und 
Klinik  der  Prostatitis  blennorrhagica  chronica.  Ibid., 
1893  (Sep.-Abdr.). — Wieaer  med.  Presse,  1893,  No.  11. 

153  Idem,  Zur  Klinik  und  pathologischen  Anatomie  der 
chronischen  Urethritis  posterior  und  Prostatitis  blennor- 
rhagica chronica.  Centralblatt  f.  d.  Krankh.  d.  Ham-  u. 
Sexualorg.,  Bd.  4,  1893,  Heft  3. 

154  Idem,  Die  Blennorrhoe  der  Sexualorgane  und  ihre  Kom- 
plikationen.      Leipzig  u.  Wien  1893. 

155  Idem,  Die  Gonokokkenpyamie.  Eine  kritisch-historische 
Studie.  Wien.  klin.  Wochenschr.,  1896,  No.  14,  p.  248 — 
252. 

156  GuiARD,  F.  P.,  Des  urethrites  latentes.  Ann.  des  mal. 
des  org.  gen.-urin.,  1884,  Fevr.,  p.  78. 

157  GuYON,  F.,  Des  prostatites  chroniques.  Lee.  clin.  rec.  par. 
E.  Desnos.      Ann.  des  mal.  gen.-urin.,  1886,  p.  382. 

158  Idem,  Prostatite  chronique.  Lee.  clin.  rec.  par  Hartmann. 
Ibid.,  1887,  p.  321 — 339. 

159  Grosglik,  Patologia  i  terapia  przewleklego  zapalenia 
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160  Haslund,  Kommunehosp.,  4.  Afd.,  i  1889.  Beretn.  om 
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93  II  615. 

161  Heisler,  Ueber  die  Zeit  und  Ursache  des  Ueberganges  der 
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162  Jamin,  Etude  sur  I'urethrite  chronique  blennorrhagique. 
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163  Jadassohn,  Beitrage  zur  Lehre  von  der  Urethritis  posterior 
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164  Idem,  Ucber  die  Behandlung  der  Gonorrhoe  mit  Argonin. 
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165  Kaufmann,  Verletzungen  und  Krankhciten  der  mann- 
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166  Koch,  Zur  Diagnose  und  Haufigkeit  der  Urethritis  pos- 
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167  Lang,  Ueber  die  Haufigkeit  und  Zeit  des  Auftretens  der 
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154 


27,  1S94.     VH.  II  706. 

168  MoNTAGNON,  De  la  frequence  dcs  localisations  et  des 
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169  Neisser,  Tagabl.  d.  Naturf.-Vers.  in  Straszburg,  1885,  P- 
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170  Ne-isser  u.  Putzler,  Zur  Bedeutung  der  gonorrhoischen 
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171  Neelsen,  Ueber  einige  histologische  Veranderungen  in  der 
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172  Neumann,  J.,  Ueber  Komplikationen  der  Urethritis. 
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173  Pezzoli,  Zur  Histologie  des  gonorrhoischen  Eiters.  Arch, 
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174  PiCARD,  Consideration  pratiques  sur  I'urethre  de  I'homme. 
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175  TouTON,  Der  Gonococcus  und  seine  Beziehung  zu  den 
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176  Wassermann  et  Halle,  Urethrite  chronique  et  retrecisse- 
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176a  Turro,  R.,  Gonokokkenzuchtung  und  kunstlicher  Tripper. 
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177  Aufrecht,  E.,  Die  diffuse  Nephritis  und  die  Entzundung 
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178  Amburger,  G.,  Ein  Fall  von  interstitieller  Nephritis. 
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179  Ballet,  Contribution  a  I'etude  du  rein  senile.  Rev.  de 
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180  Bull,  Om  kombinerte  Brightske  sygdomme.  Nordiskt 
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181  B artels,  AUgemeine  Symptomatologie  der  Nierenkrank- 
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182  Buhl,  Ueber  Bright's  Granularschwund  der  Nieren  etc. 
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183  Born,     R.,    Albuminuric    iin    Greiseanlte.      Inaug.-Diss. 


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184  Bluhm,  a.,  Zur  Aetiologie  dcs  Morbus  Brightii.  Dtsch 
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185  Brault,  a.,  Contribution  a  I'etude  des  nephrites.  These 
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1 86  Biermer,  Ueber  Nierenschrumpfung.  Breslauer  arztl. 
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187  Broadbent,  a  case  of  renal  disease  ending  in  apoplexy. 
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1 88  Crooke,  Two  cases  of  unilateral  Nephritis  with  atrophy  of 
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189  Charcot,  Maladie  de  Bright  et  nephrite  interstitielle. 
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190  Idem,  Lecons  sur  les  maladies  des  vieillards,  1868, 

191  Charcot  et  Gombault,  Nephrite  saturnine.  Arch,  de 
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192  CoRNiL  et  Brault,  Etudes  sur  la  pathologic  du  rein. 
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193  CoRNiL,  Pathologic  des  nephrites  subaigues  et  chroniques. 
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194  DuNiN,  J.,  Anatomische  Untersuchungen  uber  Nieren- 
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195  Debove  et  Letulle,  Recherches  anatomiques  et  cliniques 
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196  Demange,  Du  rein  senile.  Rev.  de  Hayem,  18S0,  p.  463 
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197  Dickinson,  W.  H.,  The  croonian  lectures  on  the  patholog\' 
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198  Idem,  Diseases  of  the  kidney  and  urinary  derangements. 
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199  Durand-Fardel,  Traite  clinique  et  pratique  des  maladies 
des  vieillards.      1854,  cf.  72. 

200  EwALD,  Ueber  Veranderungen  kleiner  Gefasze  bei  Morbus 
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201  Grawitz  u.  Israel,  Experimentelle  Untersuchungen  uber 
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202  Gull  and  Sutton,  On  the  pathology  of  the  morbid  state 
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203  Gull,  W.,  Clinical  lecture  of  chronic  Bright's  disease  with 
contracted  kidney.  Brit.  med.  Joum.,  1872,  p.  673,  707. 
VH.  II  176, 

204  Idem,  On  the  pathology  of  arterio-capillary  fibroid  kidney. 
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156 


I  261. 

205  Galabin,  On  the  connation  of  Bright's  disease  with 
changes  in  the  vascular  System.      London  1873,  nach  227. 

206  Grainger-Stewart,  Note  of  a  case  of  inflammatory 
Bright's  disease;  fatal  in  third  stage.  Brit.  med.  Journ., 
Vol.  7,  1892,  p.  27.     VH.  II  177. 

207  Idem,  On  the  inflammatory  form  of  Bright's  disease 
Med.  Tim.  and  Gaz.,  7.  VI.,  1893.     VH.  II  174. 

208  Idem,  On  a  case  of  cirrhosis  on  the  kidney.      Ibid.      VH. 

II  174. 

209  Idein,  Remarks  of  chronic  Bright's  disease,  particularly 
the  cirrhotic  form.  Brit.  med.  Journ.,  15.  IX.,  1873.  VH. 
II  174. 

210  Greenfield,  Atheroma  of  the  renal  artery  leading  to 
occlusion  of  the  vessel  and  degenerative  changes  in  th2 
kidney.      Pathol.  Trans.,  Vol.  26,  1875,  p.  135,  cf.  310. 

211  Idem,  Granular  contracted  kidney.  Path.  Trans.,  Vol. 
31,  1880,  p.  157.      VH.  I  273. 

212  GooDHART,  On  the  changes  in  the  vascular  system  in 
Bright's  disease,  deduced  from  an  analysis  of  the  post 
mortem  records  of  Guy's  Hospital  for  the  ten  years  1873 — 
1882.     Guy's  Hosp.  Rep.,  Vol.  28,  p.  103.     VH.  86  II  232. 

213  Gaucher,  E.,  Pathogenie  des  nephrites.  Paris  1886.  VH 
II  231. 

214  Guyot,  J.  G. ,  Sur  les  troubles  cardiaques  dans  la  nephrite 
interstitielle  et  de  la  cause  de  I'hypertrophie  du  coeur  dans 
cette  maladie.      Paris  1880.     VH.  II  208. 

215  HoLSTi,  Ueber  die  Veranderungen  der  feineren  Arterien 
bei  der  granularen  Nierenatrophie  und  deren  Bedeutung 
fur  die  Pathologic  dieser  Krankheit.  Dtsch.  Arch.  f. 
klin.  Med.,  Bd.  38,  1886,  p.  122 — 155. 

216  Heiberg,  Om  Morbus  Brightii.  Norsk  Magazin  for 
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217  Henouille,  De  la  nephrite  interstitielle  dans  ses  rapports 
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1876.     VH.  II  226. 

218  Hood.,     P.,    Observations    on    the   probable      causes    of 

Bright's    disease.      Lancet,    1872,    Aug.    17.     VH.    72    II 
1878. 

219  Israel,  Experimentelle  Untersuchungen  uber  den  Zusam- 
menhang  zwischen  Nierenkrankheiten  und  sekundaren 
Veranderungen  des  Cirkulationssystemes.  Virchow's 
Arch.,  Bd.  86,  1881,  p.  299 — 321. 

220  JpHNSON,  G.,  On  the  changes  in  the  blood  vessels  and  in 
the  kidney,  in  connection  with  the  small  and  granular 
kidney.  Path.  Trans.,  Vol.  28,  1877,  p.  381.  VH.  I  253. 
— Med.-chir.  Trans.,  Vol.  51,  1867,  cf.  227. 

221  Idem,  Pathology  of  chronic  Bright's  disease  with  con- 
tracted kidney  with  special  reference  to  the  theory  of 
arterio-capillary  fibrosis.  Brit.  med.  Journ.,  1872,  p.  604 
u.  695.  VH.  II  177. — Med.-chir.  Trans.,  Vol.  56,  p.  139. 
VH.  73  II  173. 

222  Idem,  A  case  of  chronic   Bright's  disease  with  rapidly 


157 


fatal  sanguineous  apoplexv.     Brit.      med.      Journ.,    1S77, 
March  9.     VH.  II  177. 

223  Idem,  On  the  nature  and  sequence  of  the  cardiac  and 
vascular  changes  in  interstitial  nephritis.  Lancet,  1881, 
April  16.      VH.  II  200. 

224  Idem,  Remarks  on  the  minute  anatomy  of  the  small  ved 
granular  kidney  Brit.  med.  Journ.,  1878,  May  25.  VH. 
II  222. 

225  Idem,  Lectures  of  the  pathology,  diagnosis  and  treatment 
of  Bright's  disease.  Ibid.,  1873,  Jan.  4,  11,  25,  Febr.  i, 
15,  22,  March  15,  22,  May  24,  June  28,  VH.  II  173. 

226  Jones,  H.  C,  Clinical  lecture  of  four  cases  of  cardy  non- 
emptying  pulse  etc.  Med.  Tim.  and  Gaz.,  1880,  p.  637, 
665.     VH.  II  158. 

227  Lemcke,  Beitrag  zur  Lehre  von  den  ursachlichen  Bezie- 
hungen  zwischen  chronischer  interstitieller  Nephritis  und 
Endarteriitis  obliterans  der  kleinen  Arterien  des  ganzen 
Korpers.  Dtsch.  Arch.  f.  klin.  Med.,  Bd.  35,  1SS4,  p. 
148—166. 

228  Lepine,  Fortschritte  der  Nierenpathologie.  Berlin  18S4, 
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229  Leyden,  Ueber  Nierenschrumpfung  und  Nierensklerose. 
Zeitschr.  f.  klin.  Med.,  Bd.  2,  1880/S1,  p.  133. 

230  LussANA,  Suir  atrofia  granulare  dei  reni.  Gaz.  med.  ital. 
lombard.,  1883,  No.  20,  22,  25,  30,  32,  1^0,  51,  1884.  VH. 
83  II  217. 

231  Lemoine,  Contribution  a  I'etude  dvi  rein  senile.  These, 
Paris  1876.      VH.  II  227. 

Wurzburg,  1891.     VFI.  II     206. 

232  Lancereaux,  Lecons  rec,  par  Boix.  i.  La  nephrite 
arterielle.  Coincidences  pathologiques.  Pathogenic; 
Lesions  consecutives  etc.  Gaz.  med.  de  Paris,  1891,  No. 
13. — 2.  La  nephrite  arterielle  chez  les  personnes  jeunes. 
Ibid.,  No.  15.     VH.  II  237. 

233  Idem,  Lecons  rec.  par  Lapierre.  Les  nephrites.  Union 
med.,  1882,  No.  64,  68,  70,  71.     VH.  II  186. 

234  Mahomed,  J.  A.,  Chronic  Bright's  disease  without  al- 
buminuria. Guy's  Hosp.  Rep.,  Vol.  25,  1881,  p.  295. 
VH.  11  199. 

235  Idem,  On  chronic  Bright's  disease  and  its  essential 
symptoms.  Lancet,  1S79,  Jan  11,  18,  Febr.  i,  22,  March 
21,  29.      VH.  II  201. — Med.-chir.  Trans.,  Vol.  57,  cf.  215. 

236  Maclagan,  The  pathology  of  the  contracting  granular 
kidney.  Brit,  and  for.  med.-chir.  Rev.,  Vol.  56,  1875, 
p.   188,  cf.  310. 

237  Meigs,  A.  V.,  Study  of  the  arteries  and  veins  in  Bright's 
disease.  Med.  Record,  New  York,  188S,  July.  VH.  I 
250. 

23S  Idem,  Chronic  endarteriitis  and  its  clinical  and  pathological 
effects  (chronic  Bright's  disease).  New  York  med.  Rec., 
1889,  Aug.      VH.  II  220. 

239  Murchison,  C,  Atrophied  kidneys,  causing  fatal  uraemia 
in  a  youth  aged  eighteen.      Trans,  of  the  path.  Soc,  Vol. 


22,    1877.   P-    177-        VH.    II    175. 

240  Petrone,  L.  M.,  L'ipertrofia  cardiaca  nella  nefrite  inter- 
stitiale  cronica.  Raccoglit.  med.,  1883,  Giugno.  VH. 
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241  Roche,  Contribution  a  I'etude  du  mouvement  de  desas- 
similation  chez  le  vieillard.      Paris  1876. 

242  Rendu,  Des  nephrites  chroniques.     These  agr.,  1878. 

243  RiNDFLEiscH,  Vcrhandlg.  d.  Kongr.  f.  innere  Med.,  Wies- 
baden 1882,  cf.  215. 

244  RosENSTEiN,  Ueberdie  verschiedenen  Formen  der  Bright's- 
chen  Krankheit.     Wien.  med.  Blatter,  1882,  No.  5 — 7. 

245  Senator,  Ueber  Schrumpfniere.  Berliner  klin.  Wochen- 
schr.,  1880,  No.  29. 

246  SoTNiTSCHEwsKY,  ViRCHow's  Arch.,  Bd.  82,  1880,  p.  209. 

247  Saundby,  The  histology  of  granular  kidney.  Path. 
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— Journ.  of  Anat.  and  Phys.,  Vol.  15,  p.  532.  VH.  80  I 
273,  II  209;    81  II  206. 

248  Sadler,  Du  rein  senile.     These  doct.,  Nancy  1879,  cf.  72,  87. 

249  Strauss  et  Germont,  Des  lesions  histologiques  du  rein 
chez  le  cobaye,  a  la  suite  de  la  ligature  de  I'uretere.  Arch, 
de  phys.,  1882,  cf.  72. 

250  ScHMAUS  u.  Horn,  Ueber  den  Ausgang  der  cyanotischen 
Induration  der  Niere  in  Granularatrophie.  Wiesbaden 
1893.     VH.  II  286. 

251  Snyers,  Pathologic  des  nephrites  chroniques.  Bruxelles 
1886.     VH.  II  230. 

252  Thoma,  Ueber  einige  senile  Veranderungen  des  mensch- 
lichen  Korpers.      Leipzig  1884.     VH.  I  226. 

253  Idem,  Zur  Kenntnis  der  Zirkulationsstorungen  in  den 
Nieren  bei  chronischer  interstitieller  Nephritis.  Virchow  's 
Arch.,  Bd.  71,  1877,  p.  227. 

254  Wagner,  Beitrage  zur  Kenntnis  des  chronischen  Morbus 
Brightii.      Arch.  f.  klin.  Med.,  Bd.  27,  1879,  p.  218. 

255  Waller,  B.  C,  On  the  nature  and  sequence  of  the  cardiac 
and  vascular  changes  in  interstitial  nephritis.  Lancet, 
Vol.  I,  r88i,  p.  208.     VH.  II  200. 

256  Weigert,  Die  BRiGHT'sche  Nierenerkrankung  vom  patho- 
logisch-anatomischen  Standpunkte.  Volkmann's  Sammlg. 
klin.  Vortr.,  No.  162 — 163,  1879. 

2=;7  Ziegler,  Ueber  die  Ursachen  der  Nierenschrumpfung  etc 
Dtsch.  Arch.  f.  klin.  Med.,  Bd.  25,  1880,  p.  585—623. 

D.  Arterial  Sclerosis  in  General — Their  Meaning, 

258  Bregman,  E..  Ein  Beitrag  zur  Kenntnis  der  Angiosklerose. 
Inaug.-Diss.  Dorpat,  1890.      VH.  91  II  137. 

259  CuRCi,  Suir  ateromasia  delle  arterie  in  rapporto  special- 
mente  alle  sue  cause  e  ai  suoi  effetti.  Lo  Sperimentale, 
1876.     VH.  II  192. 

260  CoRNiL  et  Ranvier,  Arch,  de  phys.  norm,  et  pathol.,  T. 
i,  P-  551- 


159 


26i  Crocq,  F.,  Quelques  mots  sur  rarteriosclerose.  Gaz.  hebd. 
de  med.,  1892,  No.  44,  45.      VH.  II  148. 

262  DuPLAix,  Contribution  a  I'etude  de  la  sclerose.  Paris 
1883.     VH.  I  273. 

263  DuLACSKA,  Geza,  Die  Erkrankung  der  Arterien.  Pester 
med.  Presse,  1888,  No.  44.      VH.  II  211. 

264  Ehrenreich,  Ueber  den  Bau  und  das  Wachstum  der 
innersten  Arterienhaut  und  die  Pathogenese  von  Endar- 
teriitis  chronica.      Diss.   Berlin   1880. 

265  Friedlander,  Ueber  Arteriitis  obliterans.  Centralbl.  f. 
d.  med.  Wiss.  1876,  No.  4. 

266  Idem,  Endarteriitis  obliterans.      Virchow's  Archiv,  Bd.  86. 

267  HucHARD,  H.,  Causes  et  pathogenic  de  I'arteriosclerose. 
Gaz.  hebd.  de  med.,  1889,  No.  14.      VH.  89  II  220.  _ 

268  Isnard,  De  la  sclerose  generalisee  et  du  role  de  I'arterio- 
sclerose.     Arch.  gen.  de  med.,  1886,  Fevr.      VH.  II  88. 

269  KosTER,  Pathogenese  der  Endarteriitis.  Amsterdam 
1874.      (Verslagen  etc.  der  koninkl.  Acad.,)  cf.  310,  293. 

270  KosTER,  Ueber  Endarteriitis  und  Arteriitis.  Sitzungsber. 
der  niederrhein.  Gesellsch.  f.  Natur-  u.  Heilkunde  zu  Bonn, 
20.  XII.  1875,  cf.  294. 

271  Idem,  Ueber  die  Entstehung  der  spontanen  Aneurysmen 
und  die  chronische  Mesarteriitis.  Ibid.,  19.  I.  1875,  cf. 
299.      Berl.  klin.  Wochcnschr.,  1876. 

272  Langhans,  Th.,  Beitrage  zur  normalen  und  pathologischen 
Anatomic  der  Arterien.  Virchow's  Archiv,  Bd.  36,  1866, 
p.  187 — -227. 

273  Lancereaux,  L'endarterite  ou  arteriosclerose  generalisee. 
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274  Lowenfeld,  Ueber  den  atheromatosen  Prozesz  der  Aorta. 
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275  Martin,  Recherches  sur  la  pathogenic  des  lesions  ath^ro- 
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276  Idem,  Recherches  sur  le  nature  et  la  pathogenic  des  lesions 
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277  Idem,  Considerations  generales  sur  la  pathogenie  _  des 
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278  Martha,  M.  A.,  De  la  sclerose  des  arteres.  Gaz.  des  hop., 
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279  Marchand,  Arterien.      Eulenburg's  Realencyklopadie. 

280  M'Crorie,  D.,  Atheromatous  disease  of  arteries.  Its 
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281  Mehnert,  Ueber  die  topographische  Verbreitung  der 
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z6o 


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283  Pekelharing,  Ueber  Endothelwucherung  in  Arterien. 
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284  Pernice,  Sulla  I'etiologia  del'  endarterite  chronica.  La 
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285  Peabody,  G.  L.,  Relations  between  arterial  disease  and 
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286  RoKiTANSKY,  Ucbcr  eingie  der  wichtigsten  Krankheiten 
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287  Richard,  J.,  Anatomie  pathologique  et  symptomes  de 
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288  Stroganow,  Recherches  sur  I'origine  des  elements  cellu- 
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289  Schnopfhagen,  Ueber  die  hypertrophischen  Verdickungen 
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290  Straube,  Ueber  die  Bedeutung  der  atheromatosen  Arterie- 
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291  Silbermann,  Die  diffuse  Sklerose  der  Aorta  nebst  Bemerk- 
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292  Sternfeld,  Zur  Pathogenese  und  Aetiologie  der  Athero- 
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293  Talma,  S.,  Ueber  Endarteritis  chronica.  Virchow's 
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294  Thoma,  Ueber  die  Abhangigkeit  der  Bindegewebsneu- 
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297  Birch-Hirschfeld,  Lehrbuch  der  pathologischen  Anato- 
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298  CoRNiL  et  Ranvier,  Manuel  d'histologie  pathologique. 
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302  Henle,  Handbuch  der  systematischen  Anatomic  des 
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303  Kaufmann,  E.,  Lehrb.  der  spec,  pathol.  Anatomic.  Berlin 
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304  KoLLiKER,  Gewebelehre,  1867,  p.  535.  Mikrosk.  Anatomic, 
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305  Klebs,  E.,  Handbuch  der  pathol.  Anatomic,  Bd.  i,  1876, 
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306  Lancereaux,  Traite  d'anatomic  pathologique,  1881,  II. 

307  Landois,  Handbuch  der  Physiologic,  18S9,  p.  540. 

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309  Orth,  J.,  Pathologisch-anatomische  Diagnostik,  1894,  p. 
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310  Idem,  Lehrbuch  der  specicllen  pathologischen  Anatomic 
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312  ViERORDT,  H.,  Anatomisch-physiologische  Datcn  und 
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313  Weischelbaum,  Grundrisz  der  pathologischen  Histologic, 
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314  Ziegler,  Lehrbuch  der  pathologischen  Anatomic,  7.  Aufl., 
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E.    Prostate 


315  Bruckmuller,  Pathologische  Zootomie.  Wicn  1S69,  p. 
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316  CsoKOR,  Cystenbildung  in  der  Vorstehcrdrusc  bei  einem 
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317  FoRSTER,  Handbuch  der  pathologischen  Anatomic,  2 
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318  Koch,  Encyklopadie  der  gesamtcn  Tierheilkunde,  hcraus- 
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319  KoNHAUSER,  Die  Krankheiten  des  Hundes.  Wien  1874, 
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320  MoLLER,  Lehrbuch  der  specicllen  Chirurgie  f.  Tierarzte, 
2.  Ausg.,  Stuttgart  1893,  p.  478,  468,  447. 

321  Roll,  Lehrbuch  der  Pathologic  und  Therapie  der  Haus- 
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322  Stockfleth,  Handbuch  der  tierarztlichcn  Chirurgie. 
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162 


323  Alexander,  S.,  A  suggestion  as  to  the  removal  of  ade- 
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324  AsHURST,  Philad.  med.  Times,  1882,  Vol.  13,  Dec.  2,  of.  72. 

325  Andry,  Note  sur  I'autopsie  d'un  malade  cystostomise  huit 
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II  523- 

326  Atlee,  W.  L.,  On  the  treatment  of  enlarged  prostate. 
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327  Bier,  A.,  Unterbindung  der  Art.  iliacae  internae  gegen 
Prostatahypertrophie.  Wiener  klin.  Wochenschr. ,  1893, 
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328  Bolton,  Bangs,  A  case  of  lithotrity  with  remarks  upon 
dilatation  of  the  prostate.  Annuals  of  Surgery,  1893. 
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329  BucKSTON,  Browne,  A  case  of  stiprapubic  prostatectomy. 
Lancet,  1889,  p.  487.      VH.  II  340. 

330  Idem,  Some  practical  points  in  the  treatment  of  retention 
of  urine.      Brit.  med.  Journ.,  1890,  p.  592.     VH.  II  295. 

331  Idem,  Suprapubic  prostatectomy.  Brit.  nied.  Journ., 
1893.  P-  513-     VH.  II  329. 

332  Belfield,  W.  T.,  Operations  on  the  enlarged  prostate  with 
a  tabulated  summary  of  cases.  Amer.  Journ.  of  med.  Sc, 
1890.     VH.  II  310. 

333  Bryant,  Th.,  Cases  of  prostatic  tumours  removed  in  the 
operation  of  lithotomy,  followed  by  recovery.  Trans,  of  the 
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334  Idem,  Fibrous  polypus  of  prostatic  urethra.  Lancet, 
1893,  p.  589.     VH.  11  324. 

335  Boeckel,  Des  indications  de  la  cystotomie  sus-pubienne 
'dans  les  affections  de  la  prostate.  Gaz.  med.  de  Strass- 
bourg,  VIII,  18S4,  cf.  72. 

336  Briddon,  Ch.,  Prostatectomy  by  suprapubic  incision. 
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337  BoNAN,  S.,  De  la  creation  d'une  urethre  contre  nature 
chez  les  prostatiques.  Cystostomie  suspubienne  (op. 
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93  II  329- 

338  BouTAN,  G.,  De  la  cystostomie  suspubienne.  T.  p.  1.  d., 
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339  Bazy,  Du  meat  hypogastri que  chez  les  prostatiqties.  Bull, 
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339a  BoRELius,  Behandlung  der  Prostatahypertrophie.  26. 
Kongr.  der  deutschen  Gesellsch.  f.  Chir.  Centralbl.  f. 
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340  Bron,  Le  traitement  chirurgical  des  prostatiques.  Lyon 
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341  Idem,  Sur  le  traitement  chirurgical  des  obstacles  prosta- 
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342  Bron,  F.,  Des  causes  et  du  traitement  des  valvules  urethro- 


163 


vesicales.     Lyon  med.,  1877,  No.  45  u.  46.     VH.  II  242. 

343  Bruns,  Ueber  den  gegenwartigen  Stand  der  Radikal- 
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344  Bereskin,  Chir.  Ann.,  1894,  p.  802  (russisch).      VH.II543. 
"345      Bull,  William,  Bladder  from  case  of  prostatectomy  and 

suprapubic  lithotomy.      Path.  Transact.,  Vol.  39,  p.   193. 

346  BiEDERT,  Ueber  Galvanoptmktur  der  Prostata.  Deutsche 
med.  Wochenschr.,  1888,  No.  21. 

347  BoTTiNi,  E.,  Radikale  Behandlung  der  auf  Hypertrophie 
der  Prostata  beruhenden  Ischurie.  Arch.  f.  Idin.  Chir., 
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348  Idem,  Permanente  Ischurie  wegen  Prostatahypertrophie, 
thermogalvanische  Operation.  Heilung.  Centralbl.  f. 
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348a  BoLTiNi,  E.,  Die  galvanokaustische  Diurese  zur  Radikal- 
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349  Cheron  et  MoREAU-WoLF,  Courants  continus  constants, 
des  services,  qu'ils  peuvent  rendre  dans  I'infianimation, 
I'engorgement  et  I'hypertrophie  de  le  prostate.  Gaz.  des 
hop.,   1869,  No.   150  u.  151.     VH.  I  586. 

350  Idem,  Des  services,  qui  peuvent  rendre  courants  continus 
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394- 

351  Casper,  Die  Radikalbehandlung  der  Prostatahypertrophie 
und  Prostatatumoren.  Ther.  Monatsh.,  1888,  p.  429. 
Berl.  klin.  Wochenschr.,  18S8,  No.  23  u.  24. 

352  Chance,  A.,  The  operative  treatment  of  enlarged  prostate. 
Doubl.  Journ.,  1894,  p.  359.  VH.  II  537. — Ann.  des  mal. 
gen.-urin.,  1897,  p.  018. 

353  Cameron,  H.  C.,  Prostatic  tumour  removed  by  the  supra- 
pubic operation.  Glasgow  Journ.,  1893,  p.  140.  VH.  II 
328. 

354  Clarke,  B.,  Galvanocautery  for  prostatic  obsuruction. 
Lancet,  1892,  p.  141.     VH.  II  234. 

355  Idem,  The  radical  cure  of  prostatic  obstruction  by  the 
galvanocautery.  Brit.  med.  Journ.,  1892,  p.  1327.  VH. 
II  234. 

356  CiviALE,  Traite  pratique  des  maladies  des  org.  gen.-unn 
1858 — 1860,  T.  2,  p.  338. 

357  Cabot,  Notes  on  the  non-operative  treatment  of  enlarged 
prostate.     Boston  Journ.,  4.  XII.  1890.     VH.  II  308. 

358  CzERNY,  Deutsche  med.  Wochenschr.,  1896,  No.  16. 

359  DiTTEL,  L.,  Zum  hohen  Blasenstich.  Wiener  med.  Jahrb., 
1880,  Heft  4,  Diskussion  uber  Prostatahypertrophie.  Anz. 
der  k.  k.  Ges.  d.  Aerzte  in  Wien,  No.  14. 

360  Idem,  Zur  Behandlung  der  Hypertrophie  der  Vorsteher- 
druse.      Wiener  med.  Wochenschr.,  1876,  No.  22 — 25. 

361  Idem,  Prostatectomia  lateralis.  Wiener  klin.  Wochenschr. 
1890,  No.  18  u.  19, 


164 


362  Idem,  Ein  Fall  von  Totalcxstirpation  der  Prostata.  In- 
ternat.  klin.  Rundschau,  1893,  No.  23,  p.  938.  Centralbl. 
f.  Chir.,  1893,  No.  42. 

362a  Diskussion  in  der  64.  Sitz.  der  ,, British  med.  Association" 
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363  Deneffe  et  VAN  Wetter,  De  la  ponction  de  la  vessie. 
Acad.  Royale  de  niedec,  1874,  p.  242,  532.      VH.  II  284. 

364  DiDAY,  La  neo-miction  des  cysto-stomises  etc.  Lyon 
med.,  1892,  No.  50  u.  51.      VH.  II  235. 

365  Idem,  Resultats  eloignes  de  la  cystostomie  chez  les  pros- 
tatiques.      Gaz.  hebdom.,  1893,  No.  5.      VH.  II  324. 

366  DiEULAFOY,  Traite  de  I'aspiration,  1873,  cf.  40. 

367  Desnos,  Cystotomie  et  cystostomie  chez  les  prostatiques 
Annales  des  mal.  des  org.  gen.-urin.,  1893,  p.  801. 

368  Idem,  Des  operations  palliatives  chez  les  prostatiques. 
Ann.  des  mal.  des  org.  gen.-urin.,  1894,  p.  539. 

369  Delefosse,  Rev.  crit.  Dr.  Bouton,  De  la  cystostomie 
suspubienne.      VH.  93  II  330. 

370  Davies,  J.,  The  management  of  epicystic  fistula  in  pros- 
tatic elnargement.  Amer.  News,  20.  Jan.  1894.  VH.  II 
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371  Dommes,  W.,  Radikaloperation  einer  Prostatahypertrophie 
kompliziert  mit  suppurativer  Cystitis.  Inaug.-Diss., 
Greifswald  1888.      VH.  II  334. 

372  Ebermann,  Die  Massage  der  Prostata.  Centralbl.  f.  d. 
Phys.  u.  Pathologic  der  Harn-  u.  Sexualorgane,  Bd.  3, 
1892,  p.  391. 

373  Estlander,  Kronisk  prostatitis  behandlad  need  massage 
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374  Englisch,  Ueber  die  neueren  Behandlungsmethoden  der 
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375  Eigenbrodt,  K.,  Ueber  die  Radikalbehandlung  der  Pros- 
tatahypertrophie. Beitrage  zur  klin.  Chirurgie,  Bd.  8, 
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376  Edwards,  E.,  Clinical  lecture  of  suprapubic  cystotomy. 
Med.  Tim.  and  Gaz.,  30.      V.  1885,  VH.  II  223. 

378  FoRESTiER,  Hypertrophic  totale  de  la  prostate.  Gaz.  des 
hop.,  1876,  No.  94.      VH.  II  247. 

379  V.  Frisch,  Wiener  klin.  Wochenschr.,  1896,  No.  17. 

380  Frey,  L.,  Kasuistische  Mitteil.  aus  d.  Abt.  des  Prof.  V. 
MosETiG  MooRHOF.  Rctcntio  urinae  ex  hypertrophia 
prostatae.  Blasenstich.  Injektion  von  Jodoform-Aether 
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380a  Freudenberg,  Zur  galvanokautischen  Radikalbehand- 
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381  Fenvick,  E.  H.,  Observations  on  the  effects  of  double 
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382  Fergusson,  Observations  on  lithotomy  and  on  certain 
cases  of  enlarged  prostate.  Lancet,  1S70,  Vol.  i.  VH, 
II  188.      (Path.  Soc.  of  London,  Febr.  1849.) 

383  Faulds,  a.  G.,  Castration  of  enlarged  prostate.  Brit, 
med.  Journ.,  1895,  No.  1792.  Deutsche  med.  Wochenschr. 
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384  Fehleisen,  Zur  Therapie  der  Prostatahypertrophie  und 
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385  GuYON,  "F.,  Traitement  des  prostatiques.  Ann.  des  mal. 
des  org.  gen.-urin.,  1890,  p.  i. 

386  Griffiths,  J.,  Castration  in  enlargement  of  the  prostate. 
Brit.  med.  Journ.,  1S93,  p.  765,  cf.  73. 

387  Gouley,  J.,  Some  points  in  the  surgery  of  the  hyper- 
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388  Gerrat,  Centralbl.  f.  Chir.,  1895,  No.  16. 

389  Guillemot,  Notes  sur  deux  cas  urgents  de  cystostomie 
suspubienne.      Lyon  med.,  1893,  ^O'  46-     VH.  II  324. 

390  Harrison,  Reg.  ,  Castration  in  enlargement  of  the  prostate. 
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391  Idem,  Lecturers  of  the  surgical  disorders  of  the  urinary 
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392  Idem,  On  the  restauration  of  the  function  of  micturition. 
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393  Idem,  Some  recent  advances  in  the  surgery  of  urinary 
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394  Idem,  On  the  early  treatment  of  prostatic  obstruction. 
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395  Harrison,  R.,  Prevention  of  stricture  and  of  prostatic 
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396  Howard,  Jodine  injections  of  the  hypertrophied  prostate. 
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397  Henriet,  L.,  Etude  sur  I'emploi  des  sondes  a  demeure  dans 
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398  Hogner,  R.,  On  spermatorrhoea  and  incipient  hj-per- 
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398a  Helferich,  Ueber  die  operative  Behandlung  der  Prostata- 
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399  Heine,  C.,  Ueber  Radikalbehandlung  der  Prostatahyper- 
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400  Helferich,  Ueber  operative  Versuche  zur  radikalen 
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401  Idem,  Ueber  die  Resektion  der  Samenlciter  als  eih  Heil- 
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402  Herman,  M.  W.,  O  leczeniu  przerostu  gruczolu  krokowego 
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403  JuLLiEN,  Cystotomie  et  prostatectomie  sus-pubienne. 
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404  IsNARDi,  L.,  Heilung  der  Hypertrophic  der  Prostata 
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405  Jaboulay,  La  cystostomie  suspubienne  a  travers  le  muscle 
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406  Jemoli,  Contribute  clinico  alia  cauterizzazione  ed  incisione 
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407  Jemoli,  Iscuria  da  impedimento  prostatico  curata  coUa 
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408  Krajewski,  O  doraznej  pomocy  przy  zatrzymaniu  moczu. 
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409  KoREN,  F.  i  A.,  Norsk  Magazin  for  Laegevidenskaben,  I 
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410  KuMMEL,  Die  operative  Behandlung  der  Prostatahyper- 
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411  Idem,  Die  operative  Behandlurg  der  Urinretention  bei 
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412  KoRNFELD,  Die  Behandlung  der  Prostatahypertrophie. 
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412  KoRNFELD,  Die  Behandlung  der  Prcstatahypertrophie. 
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413  KusTER,  E.,  Neue  Operationen  an  Proslata  und  Blase.  I. 
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414  Keyes,  E.  L.,  The  enlarged  prostate  and  its  operative 
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414a  KoNiG,  Beitrag  zur  operativen  Behandlung  der  Prostata- 
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4146  KoHLER,  Die  Resektion  des  Vas  defcrrrs  zur  Heilung  der 
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414c  Kohl,  Zur  Resektion  des  Vas  deferens  bei  Prostatahyper- 
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415  Kane,  Centralbl.  f.  Chir.,  1895,  No.  45. 

415a  LuNDSGAARD,  EiNAR,  Prostatahypcrtrophicns  Radicalbe- 
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416  LuTKENS,  Ein  Fall  von  Prostatahypertrophie  durch 
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417  Lawson,  Tait,  Case  of  complicated  lithotomy  successfully 
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167 


4i8  Leisrink,  Tumor  der  Prostata.  Hoher  Blasensitz.  Per- 
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419  Idem,  Beitrage  zur  Chirurgie  der  harnfuhrenden  Wege 
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420  Lane,  Considerable  hypertrophie  of  the  middle  lobe  of  tha 
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421  Lauenstein,  Die  subkutane  Durchtrennimg  des  Vas 
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422  Lewis,  Senile  hypertrophied  Prostate — retention,  prosta- 
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423  Legueu,  Note  sur  une  tumeur  pediculee  de  la  prostate. 
Ann.  des  mal.  des  org.  gen.-urin.,  1893,  p.  897. 

424  Lejars,  Sur  quatre  observations  de  cystostomie  suspu- 
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425  Lagoutte,  Prostatomie,  prostatectomie  et  cystostomie 
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426  Idem,  Resultats  eloignes  de  la  cystostomie  suspubienne 
chez  les  prostatiques  (operation  de  Poncet).  Etude 
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49.     Rf.  VH.  II  538/9. 

427  Idem,  Des  resultats  eloignes  de  la  cystostomie  suspubienne. 
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428  Moosetig-Moorhof,  Handb.  d.  chir.  Technik,  1887,  p. 
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429  Mac-Mun,  Brit.  med.  Joum.,  1S93,  Sept.  23,  cf.  73. 

430  MouLLiN,  C.  Mansell,  Castration  in  enlargement  of  the 
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431  Idem,  Lectures  of  the  operative  treatment  of  enlargement 
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432  Idem,  Two  cases  of  perineal  prostatectomy.  Lancet, 
1892,  p.  142.     VH.  II  237. 

433  Idem,  The  formation  of  a  suprapubic  urethra.  Lancet, 
1894,  June  23.      VH.  II  524. 

434  Idem,  Enlargement  of  the  prostate,  its  treatment  and 
radical  cure.      London,  VIII,  p.  526.      VH.  94  II  540. 

435  Idem,  Can  atrophy  of  the  enlarged  prostate  be  indured  by 
partial  removal.      Lancet,  1894,  p.  999.      VH.  II  540. 

436  Idem,  On  the  treatment  of  enlargement  of  the  prostate  by- 
removal  of  the  testes.  Brit.  med.  Journ.,  1894,  p.  976. 
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437  Massey,  G.  B.,  a  new  treatment  of  hypertrophie  of  the 
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438  Marchand,  Hypertrophische  Prostata.  Berl.  klin.  Wo- 
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168 


439  MiNERViNi,  Sem.  med.,  1896,  No.  21. 

440  Meyer,  Willy,  Simeltaneous  ligation  of  both  internal 
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441  Meyer  u.  Haenel,  Ein  durch  Kastration  erfolgreich  be- 
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442  McCuLLOUGH,  J.,  Senile  enlargement  of  the  prostate; 
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443  Mears,  J.  E.,  Ligatur  of  the  spermatic  cord  in  the  treat- 
ment of  hypertrophy  of  the  prostate  gland.  Philadelphia 
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444  Moses,  Therap.  Monatsh.,  1895,  Dez. 

445  Morotti,  Bottini's  galvanocaustic  treatment  of  enlarged 
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446  Idem,  Some  remarks  on  the  new  method  of  treating  en- 
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447  MusATTi,  Bericht  uber  eine  durch  thermogalvanische 
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448  Mc  Gill,  Verhandlg.  d.  10.  internat.  Kongr.,  Ill  7,  p.  98, 
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449  Idem,  A.  F.,  Suprapubische  Prostatektomie  Zuelzer's, 
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I  5,  p.  247.     VH.  89  II  339. 

450  Idem,  Discussion  on  the  treatment  of  retention  of  urine  of 
prostatic  enlargement  in  the  section  of  surgery  at  the  an- 
nual meeting  of  the  Brit.  med.  Assoc.  Brit.  med.  Journ., 
1889,  p.  807.      VH.  II  339. 

451  Molliere,  D.,  De  la  dvsurie  senile.  Lyon  med.,  1890, 
No.  12,  VH.  II  309. 

452  Manasse,  Dtsch.  med.  Wochenschr.,  1895,  No.  9,  cf.  402. 

453  Mercier,  Note  sur  la  ponction  capillaire  de  la  vessie. 
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454  Mettenheimer,  Ueber  die  v.  ScHLEiss'schen  Einreibung- 
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455  Nelaton  jun.,  Malade  opere  de  cystostomie  suspubienne 
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1894,  p.  148.     VH.  II  538. 

456  NicoLL,  Jos.  H.,  A  method  of  excising  the  prostate. 
Lancet,  1894,  p.  926.      VH.  II  541. 

457  Negretti,  Cura  radicale  dell'  iscuria  da  ipertrofia  pros- 

tatica Cauterisatione  dalla  via  rettale.      Gazz.  degli 

osped.,  1896,  No.  155. — La  sem.  med.,  1896,  No.  6,  p.  22. 

458  Obalinski,  O  doszczetnem  leczeniu  zatrzymania  moczu  u 
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lek.,  1889,  No.  37,  p.  441  (polnisch). 

459  Otis,  J.  N.,  Removal  on  the  third  lobe  of  the  prostate  with 
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Boston  Journ.,  1890,  July  3.     VH.  II  308. 

460  OswiECiMSKi,  Drei  Falle  von  seniler  Prostatahj^jertrophie, 
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461  Orcel,  Lamaladie,  lamort,  I'autopsie  de  Mr.  DiDAY.  Ann. 
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462  PowEL,   A.,   Brit.  med.  Journ.,  1893,  nov.  18,  cf.  402. 

463  Pyle,  J.  S.,  A  new  method  of  removing  the  prostate  gland. 
New  York  med.  Rec,  1892,  Aug.  6,  Centralbl.  f.  Chir., 
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464  Poncet,  Contribution  d'une  urcthre  contre  nature.  Cys- 
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465  Idem,  De  la  cystostomie  suspubienne  dans  les  accidents 
urinaires  d'origine  prostatique.  Gaz.  des  hop.,  1893,  No. 
84,  85.      VH.  93  II  325. 

466  Idem,  De  la  cystostomie  ideale  (Lecon  rec.  par  Courtillet. 
Gaz.  des  hop.,  1894,  No.  82.      VH.  94  II  323. 

467  Idem,  Indications  de  la  cystostomie  suspubienne  chez  les 
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468  Idem,  Indications  de  la  cystostomie  suspubienne  (creation 
d'une  urethre  contre  nature  temporaire  ou  permanent) 
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469  Idem,  Des  dangers  de  la  ponction  hypogastrique  dans  les 
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470  Idem,  Cystostomie  suspubienne  (creation  d'une  urethre 
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471  Pavone,  Gaz.  degli  osped.,  1895,  No.  75,  cf.  402,  423. 

472  Patteson,  Fibroglandular  hypertrophy  of  prostate.  Brit, 
med.  Journ.,  1891,  p.  288.      VH.  II  241. 

473  PoussoN,  De  1 'intervention  ehirurgicale  dans  le  diagnostic 
et  le  traitement  des  tumetirs  de  la  vessie.  These  Paris 
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474  Idem,  Des  ouvertures  chirurgicales  de  la  vessie  au  dessus 
du  pubis.  Bull,  et  Mem.  de  la  Soe.  de  Chir.,  1894,  p.  712, 
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475  Idem,  Quelques  considerations  touchant  la  valeur  de  la 
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Mercredi  medic.,  1894,  No.  52.      VH.  II  541. 

476  Ramm.  Hypei-trophia  prostatae  behandelt  mit  Kastration. 
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477  Idem,  Hypertrophia  prostatae  durch  Kastration  behandelt 
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478  Idem,  Norsk  Magazin  for  Laegevidcnskaben,  1S95,  j3-^-> 
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479  Reinert,  Versuche  uber  Organotherapie  bei  Prostata- 
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480  RiCKETTS,  Castration  for  hypertrophied  prostate.  Times 
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481  RoHMER,  de  la  cystotomie  suspubienne  dans  le  cours  de 
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482  RotrviLLE,  Un  cas  de  cystostomie  temporaire  pour  ac- 
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pellier  med.,  1893,  No.  41.     VH.  II  325. 

483  Idem,  De  I'intervention  chirurgicale  dans  I'hypertrophie 
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484  RoLLET,  Cystostomie  chez  les  prostatiques.  Arch.  prov. 
de  chir.,  1893,  p.  719.      VH.  II  329. 

485  Idem,  De  I'adherence  du  peritoine  a  la  symphyse  dans  un 
cas  de  ponction  vesicale  suivie  de  cystostomie  suspubienne. 
Lyon  med.,  1894,  No.  3.      VH.  II  524. 

486  Rosenberg,  Die  Therapie  der  Prostatitis  chronica.  Cen- 
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487  RoBSON,  A.  W.,  Suprapubic  prostatectomy  or  Mc  Gill's 
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488  Remy,  M.,  Traitement  d'urgence  de  la  retention  d'urine 
chez  les  prostatiques.  Bull.  Therap.,  1894,  Janv.  15. 
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489  Roth,  Ischurie  dans  un  cas  d 'hypertrophic  de  la  prostate. 
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490  Swain,  Castration  for  prostatic  hj^pertrophy.  Brit.  med. 
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491  SouTHAM,  F.  A.,  A  case  of  prostatic  retention  of  urine 
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492  Schmidt,  Hans,  Prostatectomia  alta.  Festschr.  z.  Feier 
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493  Schmidt,  Meinhardt,  Zur  operativen  Behandlung  der 
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494  Schmidt,  Benno,  Operative  Behandlung  der  hypertro- 
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495  Senn,  N.,  Self-retaining  drainage-tube  after  suprapubic 
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496  Szuman,  L.,  Leczenie  przerostu  gruczolu  krokowego  u 
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497  Sacaze,  Dc  la  cystotomie  suspubienne  dans  I'hypertrophie 
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239- 

498  ScHUSTLER,  M.,  Zur  opcrativen  Bchandlung  dcr  Prostata- 
hvpertrophie.  Wien.  klin.  Wochenschr.,  1888,  No.  17. 
VH.  II  334. 

499  Sansini,  Iscuria  permanentc  da  ipertrofia  prostatica, 
cauterisazione  tcrmogalvanica  della  prostata.  Guarigione. 
Gaz.  lombard.,  188S,  No.  23.     VH.  II  333. 

499a  Sawicki,  B.,  O  leczeniu  przerostu  gruczolu  krokowego 
zapomoca  rekoczynow  operacyjnych.  Gaz.  lek.,  1895, 
No.  23  i  24  (polnisch). 

500  SussKiND,  A.,  Ueber  die  Behandlung  der  Prostatahyper- 
trophie.  Wurttemb.  Korresp. -Blatter,  1885,  Nov.  2. 
VH.  II  231. 

501  Spanton,  Large  sarcomatous  tumour  of  prostate  gland; 
excision;  fatal  result,  remarks.  Lancet,  1882,  p.  1033. 
VH.  II  205. 

502  ToBiN,  R.,  Resection  of  the  prostate  gland  for  enlarge- 
ment causing  retention  of  urine.  Brit.  med.  Journ.,  1891, 
March  14.      VH.  90  II  308. 

503  Idem,  Prostatectomy  for  senile  prostatic  enlargement. 
Doublin  Journ.,  1891,  p.  497.      VH.  II  241. 

504  TuFFiER,  Prostatectomie  par  la  voie  suspubienne.  Bull, 
et  Mem.  de  la  Soc.  de  Chir.,  Paris  1892,  p.  842.  VH.  93 
II  326. 

505  Thure-Brandt,  Zur  Massage  bei  Prostatitis.  Dtsch.  med. 
Wochenschr.,  1892,  No.  44,  p.  990.  Idem,  Nachtrag,  ibid.. 
No.  51 ,  p.  1 166. 

506  Tripier,  a.,  Traitement  de  1 'hypertrophic  prostatique  par 
I'electricite.  Compt.  rend,  de  I'acad.  de  sciences,  1859, 
T.  49,  p.  219. 

507  Thomas,  J.  D.,  Removal  of  both  testicles  for  chronic 
hypertrophy  of  prostata.  Philadelphia  Rep.,  1894,  Dec. 
29,  VH.  II  542. 

508  Taylor,  B.  W.,  Suprapubic  cystotomy  for  prostated  en- 
largement.     Ainer.  News,  1894,  Febr.  5.      VH.  II  538. 

509  Ulatowski,  O  zatrzymaniu  moczu  i  usunieciu  takowego 
sposobem  wyssania  trojgrancem  wloskowatym.  Nowiny 
lekarskie,  1890,  No.  6,  7  (polnisch). 

510  ViGNARD,  Des  operations  palliatives  chez  les  prostatiques. 
Ann.  des  mal.  des  org.  gen.-urin.,  1890,  Nov.,  p.  649. 
VH.  II  311. 

511  Idem,  De  la  prostatatomie  et  de  la  prostatectomie  et  en 
particulier  de  leurs  indications.  These  Paris  1890.  VH. 
II  309. 

512  Watson,  S.  F.,  The  operative  treatment  of  the  hyper- 
trophied  prostate.  Ann.  of  Surgery,  Vol.  9,  1889,  p.  i — 
29,  Centralbl.  f.  Chir.,  1889,  No.  24.      VH.  II  309. 

513  Idem,  A  case  suggesting  the  advantage  of  repeated  supra- 
pubic aspirations  of  the  bladder  as  compared  with  cathe- 
terisation  for  the  relief  of  retention  of  urine  due  to  prostatic 
hypertrophic.      Boston    Journ.,     1891,    p.    687.     VH.     II 

239- 

514  WiESiNGER,  A.,  Dtsch.  Zeitschr.  f.  Chir.,  Bd.  42,  Heft  2. 


172 


515  Wattelet,  Ponction  de  la  vessie  par  aspiration.  Paris 
1871,  cf.  40. 

516  Weir,  On  cystotomy  for  cystitis  in  the  male.  New  York 
med.  Rec,  Vol.  17,  1880,  cf.  72. 

517  Williams,  Brit.  med.  Journ.,  1S78,  cf.  72. 

518  Weller,  van  Hook,  Two  prostatectomies.  Amer.  News, 
1893,  Nov.  25.     VH.  II  326. 

519  Wassilieff,  Cystostomie  ideale.  Gaz.  des  hop.,  1894. 
No.  45-      VH.  II  523. 

520  WiSHARD,  W.  N.,  Notes  of  the  surgery  of  the  prostate. 
Journ.  of  cut.  and  genit.-urin.  diseases,  1892,  No.  3,  Cen- 
tralbl.  f.  Chir.,  1893,  No.  2.      VH.  92  II  235/6. 

521  White,  W.,  Castration  for  the  case  of  hypertrophied. 
prostate.  Brit.  med.  Journ.,  23.  VI.  1894.  Ther.  Monatsh., 
1895,  No.  I.  Brit.  med.  Journ.,  5.  I.  1895.  Centralbl.  f, 
Chir.,  No.  23. 

522  Idem,  La  castration  pour  1 'hypertrophic  de  la  prostate. 
Union  med.,  1897,  No.  74.      VH.  II  542.     Vergl.  auch  A). 

523  Idem,  Two  cases  of  prostatectomy.  Amer.  News,  Dec. 
13,  1890.     VH.  309. 

524  Idem,  A  case  of  suprapubic  lithotomy  and  prostatectomy. 
Brit.  med.  Journ.,  July  3,  1890.     VH.  II  309 

525  Idem,  A  summary  of  the  history  and  present  position  of 
the  operation  of  castration  for  hypertrophy  of  the  prostate. 
Med.  News,  June  4,  Boston  Journ.,  Aug.  23,  Brit.  med. 
Journ.,  June  23,  1894.     VH.  II  542. 

526  Idem,  The  results  of  double  castration.  Ann.  of  Surg., 
VII.  1895.  Centralbl.  f.  Chir.,  1895,  No.  40.  Med.  News, 
8.  VI.  1895. 

527  ZiEMBicKi,  Retention  d'urine  traitee  par  la  taille  hypo- 
gastrique  et  la  resection  des  trois  lobes  de  la  prostate. 
Ann.  des  mal.  des  org.  gen.-urin.,  1891,  p.  409.  (VH.  II 
238,  241.)      Separatabdruck. 

528  Zaleski,  a.,  Leczenie  doszczetne  przerostu  starczego 
gruczolu  krokowego.  Kronika  lekarska,  1896,  Heft  11 — 
13  (polnisch). 


173 


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175 


Date  Due 

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